Gastritis pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
m (Bot: Removing from Primary care)
 
(10 intermediate revisions by 3 users not shown)
Line 4: Line 4:


==Overview==
==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 infection|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 [[Ischemia|ischemic]] damage. In chronic gastritis, the ''[[H. pylori]]'' infection persists leading to accumulation of large number [[chronic]] [[inflammatory cells]] leading to active chronic gastritis.
Gastritis depending on the causes may be classified into [[acute gastritis]], chronic gastritis, [[atrophic gastritis]], and [[H. pylori|H. pylori]] associated gastritis. In the majority of patients with acute gastritis, the initial acute phase of [[gastritis]] is [[subclinical infection|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 [[Ischemia|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==
==Pathophysiology==
===Acute gastritis===
===Acute gastritis===
*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 [[Ischemia|ischemic]] damage. The outcome of these triggers may result in ulcers, hemorrhage and erosion of the gastric mucosa.
====Pathogenesis====
*The decrease in the [[prostaglandin]] synthesis is thought to be the reason for the injury to the [[gastric mucosa]]. The [[gastric mucosa]] is safeguarded from the deleterious effects of the [[gastric acid]] by mechanisms promoted by the [[prostaglandins]].
*In the majority of patients, the initial acute phase of [[gastritis]] is [[subclinical infection|subclinical]] and is of short duration (about 7 to 10 days).
*In the majority of patients, the initial acute phase of [[gastritis]] is [[subclinical infection|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 [[Ischemia|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.<ref name="pmid1752479">{{cite journal| author=Sobala GM, Crabtree JE, Dixon MF, Schorah CJ, Taylor JD, Rathbone BJ et al.| title=Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations. | journal=Gut | year= 1991 | volume= 32 | issue= 11 | pages= 1415-8 | pmid=1752479 | doi= | pmc=1379180 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1752479  }} </ref> In [[H. pylori]] infection, the organisms are spontaneously cleared in a small minority of people, especially in childhood.
*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.<ref name="pmid1752479">{{cite journal| author=Sobala GM, Crabtree JE, Dixon MF, Schorah CJ, Taylor JD, Rathbone BJ et al.| title=Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations. | journal=Gut | year= 1991 | volume= 32 | issue= 11 | pages= 1415-8 | pmid=1752479 | doi= | pmc=1379180 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1752479  }} </ref>
*Following transmission, [[H. pylori]] penetrates the [[gastric mucosa]] and multiplies close to the surface [[epithelial cells]].  
*In ''[[H. pylori]]'' infection, the organisms are spontaneously cleared in a small minority of people, especially in childhood.
 
====Pathogenesis====
*Following transmission, ''[[H. pylori]]'' penetrates the [[gastric mucosa]] and multiplies close to the surface [[epithelial cells]].
*Following adhesion to [[epithelial cells]], the [[bacteria]] releases [[lipopolysaccharides]] ([[endotoxin]]) and [[chemotaxis|chemotactic mediators]] which penetrate the surface epithelial cells.<ref name="pmid9861460">{{cite journal| author=Slomiany BL, Piotrowski J, Slomiany A| title=Induction of caspase-3 and nitric oxide synthase-2 during gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide. | journal=Biochem Mol Biol Int | year= 1998 | volume= 46 | issue= 5 | pages= 1063-70 | pmid=9861460 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9861460  }} </ref><ref name="pmid8730257">{{cite journal| author=Crabtree JE| title=Gastric mucosal inflammatory responses to Helicobacter pylori. | journal=Aliment Pharmacol Ther | year= 1996 | volume= 10 Suppl 1 | issue=  | pages= 29-37 | pmid=8730257 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8730257  }} </ref>
*Following adhesion to [[epithelial cells]], the [[bacteria]] releases [[lipopolysaccharides]] ([[endotoxin]]) and [[chemotaxis|chemotactic mediators]] which penetrate the surface epithelial cells.<ref name="pmid9861460">{{cite journal| author=Slomiany BL, Piotrowski J, Slomiany A| title=Induction of caspase-3 and nitric oxide synthase-2 during gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide. | journal=Biochem Mol Biol Int | year= 1998 | volume= 46 | issue= 5 | pages= 1063-70 | pmid=9861460 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9861460  }} </ref><ref name="pmid8730257">{{cite journal| author=Crabtree JE| title=Gastric mucosal inflammatory responses to Helicobacter pylori. | journal=Aliment Pharmacol Ther | year= 1996 | volume= 10 Suppl 1 | issue=  | pages= 29-37 | pmid=8730257 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8730257  }} </ref>
*These bacterial factors attract the [[polymorphonuclear leukocytes]] to the site of [[infection]] and also caused [[degranulation|mast cell degranulation]], which releases acute inflammatory mediators. [[Degranulation|Mast cell degranulation]] leads to:
:*Increased [[vascular permeability]]
:*Increased [[polymorphonuclear leukocytes]] [[emigration]]
:*Increased expression of [[cell adhesion molecules|leukocyte adhesion molecules]]
:*The [[platelet activating factor|platelet activating factors (PAF)]] released from [[mast cells]] causes [[thrombosis|microthrombosis]] in [[capillary|mucosal capillaries]] resulting in [[hypoxia|hypoxic injury]] to the [[epithelium]]
*The [[macrophages]] release [[IL-1]] and [[tumor necrosis factor alpha|tumor necrosis factor alpha (TNF-α)]] which stimulates gastric epithelium to produce [[IL-8]].
*The acute phase is associated with profound [[hypochlorhydria]] and a decreased [[ascorbic acid]] secretion into the [[gastric juice]].<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949  }} </ref>
*The acid output reaches pre-infection levels after several weeks but the [[ascorbic acid]] remains lower than normal for the duration of [[chronic]] [[gastritis]], indicating that it is due to persisting [[inflammation]] rather than [[hypochlorhydria]].<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949  }} </ref>


====Microscopic pathology====
====Microscopic pathology====


Histological features observed such as:
Histological features observed includes:
*[[Hyperemia]]
*[[Hyperemia]]
*[[Acute]] [[inflammation]]
*[[Acute]] [[inflammation]]
Line 37: Line 28:


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


====Pathogenesis====
====Pathogenesis====
*The major diagnostic feature of chronic gastritis is an influx of [[lymphocytes]] and [[plasma cells]] (normally the antral mucosa is devoid of [[plasma cells]] and [[lymphocytes]]). Hence the presence of these cells is indicative of [[gastritis]].<ref name="pmid8505036">{{cite journal| author=Genta RM, Hamner HW, Graham DY| title=Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy. | journal=Hum Pathol | year= 1993 | volume= 24 | issue= 6 | pages= 577-83 | pmid=8505036 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8505036  }} </ref>
*The major diagnostic feature of chronic gastritis is an influx of [[lymphocytes]] and [[plasma cells]] (normally the antral mucosa is devoid of [[plasma cells]] and [[lymphocytes]]). Hence the presence of these cells is indicative of [[gastritis]].<ref name="pmid8505036">{{cite journal| author=Genta RM, Hamner HW, Graham DY| title=Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy. | journal=Hum Pathol | year= 1993 | volume= 24 | issue= 6 | pages= 577-83 | pmid=8505036 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8505036  }} </ref>
*[[H. pylori|''H. pylori'']] colonizes more in the [[antrum]] than the corpus. Hence there is increased [[inflammatory cell]] infiltration in the antrum.
*[[H. pylori|H. pylori]] colonizes more in the [[antrum]] than the corpus. Hence there is increased [[inflammatory cell]] infiltration in the antrum.
*The direct acting [[antigens]] of ''[[H. pylori]]'' like [[lipopolysaccharides]], [[urease]] etc along with [[interleukins|interleukins 1 and 6]], activate [[T-helper cells]] which produce the variety of [[cytokines]] including IL4, IL5, and IL6.
*The direct acting [[antigens]] of [[H. pylori]] like [[lipopolysaccharides]] and [[urease]] along with [[interleukins|interleukins 1 and 6]], activate [[T-helper cells]] which produce the variety of [[cytokines]] including IL-4, IL-5, and IL-6.
*These [[interleukins]] differentiate into [[plasma cells]] releasing [[cytokines]] and anti-H.pylori infection like [[opsonization|IgM-opsonizing]] and [[complement]]-fixing antibodies.  
*These [[interleukins]] differentiate into [[plasma cells]] releasing [[cytokines]] and anti-H.pylori infection like [[opsonization|IgM-opsonizing]] and [[complement]]-fixing antibodies.  
*The main role of the [[mucosa]] in the [[immune]] response is that the [[IgA]] prevents [[bacterial]] [[adhesion]] and [[IgG]] causes [[opsonization]] and [[complement]] activation.
*The main role of the [[mucosa]] in the [[immune]] response is that the [[IgA]] prevents [[bacterial]] [[adhesion]] and [[IgG]] causes [[opsonization]] and [[complement]] activation.
*Due to the acidic environment, the [[antibodies]] produced quickly lose their adhesive properties and [[catalase]] produced by ''[[H. pylori]]'' protects against polymorphs.
*Due to the acidic environment, the [[antibodies]] produced quickly lose their adhesive properties and [[catalase]] produced by [[H. pylori]] protects against polymorphs.
*However, this [[immune response]] is insufficient to eradicate the organism leading to the development of immune response directed towards preventing the damaging effects of the ''[[H. pylori]]''.
*However, this [[immune response]] is insufficient to eradicate the organism leading to the development of immune response directed towards preventing the damaging effects of the [[H. pylori]].
*Hence the persistent [[antigenic]] stimulation leads to the formation of [[lymphoid follicles]], which is the consistent feature of chronic ''[[H. pylori]]'' infection.
*Hence the persistent [[antigenic]] stimulation leads to the formation of [[lymphoid follicles]], which is the consistent feature of chronic [[H. pylori]] infection.
*These [[lymphoid follicles]] in the [[gastric mucosa]] constitutes [[MALT|mucosa-associated lymphoid tissue (MALT)]] from which gastric [[marginal zone]] [[B-cell lymphoma|B-cell lymphoma (MALToma)]] arises.
*These [[lymphoid follicles]] in the [[gastric mucosa]] constitutes [[MALT|mucosa-associated lymphoid tissue (MALT)]] from which gastric [[marginal zone]] [[B-cell lymphoma|B-cell lymphoma (MALToma)]] arises.
Also, these polymorphs accumulate around the pit isthmus, which is a proliferative compartment, causing lethal damage to [[stem cells]] resulting in [[glandular]] [[atrophy]].
Also, these polymorphs accumulate around the pit isthmus, which is a proliferative compartment, causing lethal damage to [[stem cells]] resulting in [[glandular]] [[atrophy]].
Line 54: Line 45:
*Variable epithelial [[degeneration]]
*Variable epithelial [[degeneration]]
*[[Neutrophil]] infiltration in the epithelium and the [[lamina propria]]
*[[Neutrophil]] infiltration in the epithelium and the [[lamina propria]]
*Variable ''[[H. pylori]]'' colonization
*Variable [[H. pylori]] colonization
*[[Lymphocytes]] and [[plasma cell]] infiltration
*[[Lymphocytes]] and [[plasma cell]] infiltration
*[[Lymphoid follicles]] (typical feature of chronic gastritis)
*[[Lymphoid follicles]] (typical feature of chronic gastritis)
Line 113: Line 104:
===Atrophic Gastritis===
===Atrophic Gastritis===
[[Atrophy]] of [[stomach]] is defined as loss of [[glandular]] tissue due to continuous [[mucosal]] injury. This leads to thinning of [[gastric mucosa]].
[[Atrophy]] of [[stomach]] is defined as loss of [[glandular]] tissue due to continuous [[mucosal]] injury. This leads to thinning of [[gastric mucosa]].
*The [[prevalence]] and severity of [[atrophy]] of [[stomach]] increases with age among the patient's [[chronic]] [[gastritis]] due to longer duration of ''[[H. pylori]]'' infection.
*The [[prevalence]] and severity of [[atrophy]] of [[stomach]] increases with age among the patient's [[chronic]] [[gastritis]] due to longer duration of [[H. pylori]] infection.
*Due to glandular [[atrophy]], the prevalence of ''[[H. pylori]]'' positivity decreases. The main reasons are as follows:
*Due to glandular [[atrophy]], the prevalence of [[H. pylori]] positivity decreases. The main reasons are as follows:
:*Due to [[intestinal]] [[metaplasia]] that is usually present in [[atrophic]] [[stomach]], the organisms are absent as they usually colonize only [[gastric]] [[epithelium]].
:*Due to [[intestinal]] [[metaplasia]] that is usually present in [[atrophic]] [[stomach]], the organisms are absent as they usually colonize only [[gastric]] [[epithelium]].
:*As ''[[H. pylori]]'' requires partially acidic environment to thrive, [[hypochlorhydria]] creats hostile environment to ''[[H. pylori]]'' to survive.<ref name="pmid1916500">{{cite journal| author=Neithercut WD, Milne A, Chittajallu RS, el Nujumi AM, McColl KE| title=Detection of Helicobacter pylori infection of the gastric mucosa by measurement of gastric aspirate ammonium and urea concentrations. | journal=Gut | year= 1991 | volume= 32 | issue= 9 | pages= 973-6 | pmid=1916500 | doi= | pmc=1379031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1916500  }} </ref>
:*As [[H. pylori]] requires partially acidic environment to thrive, [[hypochlorhydria]] creates hostile environment to [[H. pylori]] to survive.<ref name="pmid1916500">{{cite journal| author=Neithercut WD, Milne A, Chittajallu RS, el Nujumi AM, McColl KE| title=Detection of Helicobacter pylori infection of the gastric mucosa by measurement of gastric aspirate ammonium and urea concentrations. | journal=Gut | year= 1991 | volume= 32 | issue= 9 | pages= 973-6 | pmid=1916500 | doi= | pmc=1379031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1916500  }} </ref>
:*The [[metaplasia|metaplastic epithelium]] secretes acidic [[glycoproteins]] which create the most hostile environment for ''[[H. pylori]]''.
:*The [[metaplasia|metaplastic epithelium]] secretes acidic [[glycoproteins]] which create the most hostile environment for [[H. pylori]].
*Hence, based on above reasons, failure to demonstrate ''[[H. pylori]]'' does not deny the role of the organism in [[atrophic gastritis]].
*Hence, based on above reasons, failure to demonstrate [[H. pylori]] does not deny the role of the organism in [[atrophic gastritis]].


====Pathogenesis====
====Pathogenesis====
*The continuous mucosal injury due to long-standing ''[[H. pylori]] i''nfection, leads to [[atrophy]] of stomach.
*The continuous mucosal injury due to long-standing [[H. pylori]] infection, leads to [[atrophy]] of stomach.
*This continuous pathological process results in [[gastric erosion|erosion]] or [[ulcer|ulceration]] of the [[mucosa]] leading to the destruction of the [[glandular]] layer and followed by [[fibrous]] replacement.
*This continuous pathological process results in [[gastric erosion|erosion]] or [[ulcer|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 [[metaplasia|metaplastic glands]] (pseudo-[[pyloric]] appearance) which are composed of cells of the 'ulcer-associated cell lineage' (UACL).<ref name="pmid11358897">{{cite journal| author=Pera M, Heppell J, Poulsom R, Teixeira FV, Williams J| title=Ulcer associated cell lineage glands expressing trefoil peptide genes are induced by chronic ulceration in ileal pouch mucosa. | journal=Gut | year= 2001 | volume= 48 | issue= 6 | pages= 792-6 | pmid=11358897 | doi= | pmc=1728308 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11358897  }} </ref>
*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 [[metaplasia|metaplastic glands]] (pseudo-[[pyloric]] appearance) which are composed of cells of the 'ulcer-associated cell lineage' (UACL).<ref name="pmid11358897">{{cite journal| author=Pera M, Heppell J, Poulsom R, Teixeira FV, Williams J| title=Ulcer associated cell lineage glands expressing trefoil peptide genes are induced by chronic ulceration in ileal pouch mucosa. | journal=Gut | year= 2001 | volume= 48 | issue= 6 | pages= 792-6 | pmid=11358897 | doi= | pmc=1728308 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11358897  }} </ref>
Line 128: Line 119:
*Reduced number of [[oxyntic cells]]. No intestinal [[metaplasia]]
*Reduced number of [[oxyntic cells]]. No intestinal [[metaplasia]]
*The [[mucosa]] is infiltrated with [[neutrophils]]
*The [[mucosa]] is infiltrated with [[neutrophils]]
*''[[H. pylori]]'' is not seen on [[H&E stain]].
*[[H. pylori]] is not seen on [[H&E stain]].
*[[Immunohistochemical]] stain of ''[[H. pylori]]'' detects the organisms.
*[[Immunohistochemical]] stain of [[H. pylori]] detects the organisms.


[[image:Atrophic_gastritis.jpg|thumb|200px|center|Atrophic Gastritis, By Radioxoma (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons<ref name="urlFile:Atrophic gastritis (low zoom).jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AAtrophic_gastritis_(low_zoom).jpg |title=File:Atrophic gastritis (low zoom).jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>]]
[[image:Atrophic_gastritis.jpg|thumb|200px|center|Atrophic Gastritis, By Radioxoma (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons<ref name="urlFile:Atrophic gastritis (low zoom).jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AAtrophic_gastritis_(low_zoom).jpg |title=File:Atrophic gastritis (low zoom).jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>]]
Line 135: Line 126:
==Gross pathology==
==Gross pathology==
*'''Erosive Gastritis:'''
*'''Erosive Gastritis:'''
**Erosive gastritis results due to the loss of [[superficial]] [[epithelium]] causing and it does not extend beyond the [[muscularis]] [[mucosa]].
**Erosive gastritis results due to the loss of [[superficial]] [[epithelium]], it usually does not extend beyond the [[muscularis]] [[mucosa]].
**The crypts may present as [[dilated]] and contain acute [[inflammatory]] cells.
**The crypts may present as [[dilated|dilatations]] and contain acute [[inflammatory]] cells.
[[image:Gastritis_erosiva.2278.jpg|thumb|300px|center|Erosive Gastritis, By Amadalvarez (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons<ref name="urlFile:Gastritis erosiva.2278.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AGastritis_erosiva.2278.jpg |title=File:Gastritis erosiva.2278.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>]]
[[image:Gastritis_erosiva.2278.jpg|thumb|300px|center|Erosive Gastritis, By Amadalvarez (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons<ref name="urlFile:Gastritis erosiva.2278.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AGastritis_erosiva.2278.jpg |title=File:Gastritis erosiva.2278.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>]]


Line 149: Line 140:
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
[[Category:Gastroenterology]]
​​
 
{{WH}}
{{WH}}
{{WS}}
{{WS}}
[[Category:Medicine]]
[[Category:Gastroenterology]]
[[Category:Up-To-Date]]

Latest revision as of 21:49, 29 July 2020

Gastritis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Gastritis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Diagnostic tests

Endoscopic tests
Nonendoscopic tests

X Ray

CT

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Gastritis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Gastritis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Gastritis pathophysiology

CDC on Gastritis pathophysiology

Gastritis pathophysiology in the news

Blogs on Gastritis pathophysiology

Directions to Hospitals Treating Gastritis

Risk calculators and risk factors for Gastritis pathophysiology

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 the majority of patients with acute gastritis, 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

Pathogenesis

Microscopic pathology

Histological features observed includes:

Chronic gastritis

In the majority of cases, the H. pylori infection persists leading to accumulation of large number of 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[8]

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
  • 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).[10]

Microscopic pathology

Atrophic Gastritis, By Radioxoma (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons[11]

Gross pathology

Erosive Gastritis, By Amadalvarez (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons[12]

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. ↑ 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.
  5. ↑ 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.
  6. ↑ "File:Chronic gastritis -- intermed mag.jpg - Wikimedia Commons".
  7. ↑ "File:Chronic gastritis -- very high mag.jpg - Wikimedia Commons".
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ "File:Atrophic gastritis (low zoom).jpg - Wikimedia Commons".
  12. ↑ "File:Gastritis erosiva.2278.jpg - Wikimedia Commons".

​​ Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Gastritis_pathophysiology&oldid=1638409"