Upper gastrointestinal bleeding pathophysiology: Difference between revisions

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{{CMG}}; {{AE}} {{ADG}}
{{CMG}}; {{AE}} {{ADG}}
==Overview==
==Overview==
The main inciting event in the pathogenesis of upper GI bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to [[ligament of Treitz]], it is defined as upper GI bleeding. Regardless of etiology, if the balance of [[gastric acid]] secretion and mucosal defenses is disrupted, [[acid]] interacts with the [[epithelium]] to cause damage.
The main inciting event in the pathogenesis of upper gastrointestinal (GI) bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to [[ligament of Treitz]], it is defined as upper GI bleeding. Regardless of etiology, if the balance of [[gastric acid]] secretion and mucosal defenses is disrupted, [[acid]] interacts with the [[epithelium]] to cause damage.


==Pathophysiology==
==Pathophysiology==


===Blood supply of Foregut===
===Blood Supply of Foregut===
The digestive system is supplied by the [[celiac artery]]. The [[celiac artery]] is the first major branch from the [[abdominal aorta]], and is the only major [[artery]] that supplies the digestive organs.<ref name="pmid18730308">{{cite journal |vauthors=Feldman SE |title=Blood supply to stomach |journal=Calif Med |volume=112 |issue=4 |pages=55 |year=1970 |pmid=18730308 |pmc=1501289 |doi= |url=}}</ref><ref name="pmid26140727">{{cite journal |vauthors=Granger DN, Holm L, Kvietys P |title=The Gastrointestinal Circulation: Physiology and Pathophysiology |journal=Compr Physiol |volume=5 |issue=3 |pages=1541–83 |year=2015 |pmid=26140727 |doi=10.1002/cphy.c150007 |url=}}</ref><ref name="pmid11355897">{{cite journal |vauthors=Geboes K, Geboes KP, Maleux G |title=Vascular anatomy of the gastrointestinal tract |journal=Best Pract Res Clin Gastroenterol |volume=15 |issue=1 |pages=1–14 |year=2001 |pmid=11355897 |doi=10.1053/bega.2000.0152 |url=}}</ref><ref name="pmid986621">{{cite journal |vauthors=Varga F, Csáky TZ |title=Changes in the blood supply of the gastrointestinal tract in rats with age |journal=Pflugers Arch. |volume=364 |issue=2 |pages=129–33 |year=1976 |pmid=986621 |doi= |url=}}</ref><ref name="pmid4599528">{{cite journal |vauthors=Matuchansky C, Bernier JJ |title=[Prostaglandins and the digestive tract] |language=French |journal=Biol Gastroenterol (Paris) |volume=6 |issue=3 |pages=251–68 |year=1973 |pmid=4599528 |doi= |url=}}</ref><ref name="pmid4372738">{{cite journal |vauthors=Radbil' OS |title=[Prostaglandins and the digestive system organs] |language=Russian |journal=Ter. Arkh. |volume=46 |issue=4 |pages=6–14 |year=1974 |pmid=4372738 |doi= |url=}}</ref><ref name="pmid6990725">{{cite journal |vauthors=Robert A |title=Prostaglandins and digestive diseases |journal=Adv Prostaglandin Thromboxane Res |volume=8 |issue= |pages=1533–41 |year=1980 |pmid=6990725 |doi= |url=}}</ref>
The digestive system is supplied by the [[celiac artery]]. The [[celiac artery]] is the first major branch from the [[abdominal aorta]], and is the only major [[artery]] that supplies the digestive organs.<ref name="pmid18730308">{{cite journal |vauthors=Feldman SE |title=Blood supply to stomach |journal=Calif Med |volume=112 |issue=4 |pages=55 |year=1970 |pmid=18730308 |pmc=1501289 |doi= |url=}}</ref><ref name="pmid26140727">{{cite journal |vauthors=Granger DN, Holm L, Kvietys P |title=The Gastrointestinal Circulation: Physiology and Pathophysiology |journal=Compr Physiol |volume=5 |issue=3 |pages=1541–83 |year=2015 |pmid=26140727 |doi=10.1002/cphy.c150007 |url=}}</ref><ref name="pmid11355897">{{cite journal |vauthors=Geboes K, Geboes KP, Maleux G |title=Vascular anatomy of the gastrointestinal tract |journal=Best Pract Res Clin Gastroenterol |volume=15 |issue=1 |pages=1–14 |year=2001 |pmid=11355897 |doi=10.1053/bega.2000.0152 |url=}}</ref><ref name="pmid986621">{{cite journal |vauthors=Varga F, Csáky TZ |title=Changes in the blood supply of the gastrointestinal tract in rats with age |journal=Pflugers Arch. |volume=364 |issue=2 |pages=129–33 |year=1976 |pmid=986621 |doi= |url=}}</ref><ref name="pmid4599528">{{cite journal |vauthors=Matuchansky C, Bernier JJ |title=[Prostaglandins and the digestive tract] |language=French |journal=Biol Gastroenterol (Paris) |volume=6 |issue=3 |pages=251–68 |year=1973 |pmid=4599528 |doi= |url=}}</ref><ref name="pmid4372738">{{cite journal |vauthors=Radbil' OS |title=[Prostaglandins and the digestive system organs] |language=Russian |journal=Ter. Arkh. |volume=46 |issue=4 |pages=6–14 |year=1974 |pmid=4372738 |doi= |url=}}</ref><ref name="pmid6990725">{{cite journal |vauthors=Robert A |title=Prostaglandins and digestive diseases |journal=Adv Prostaglandin Thromboxane Res |volume=8 |issue= |pages=1533–41 |year=1980 |pmid=6990725 |doi= |url=}}</ref>
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
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| rowspan="3" |'''<u>[[Esophagus]]</u>'''
| rowspan="3" |'''<u>[[Esophagus]]</u>'''
|
|
[[Upper esophageal sphincter]]<br>  
[[Upper esophageal sphincter]]<br> [[Esophagus|Cervical esophagus]]
[[Esophagus|Cervical esophagus]] 
| [[Inferior thyroid artery]] 
| [[Inferior thyroid artery]] 
|-
|-
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|-
|-
|
|
[[Esophagus|Distal esophagus]]<br>
[[Esophagus|Distal esophagus]]<br>[[Lower esophageal sphincter]]
[[Lower esophageal sphincter]]
|[[Left gastric artery]] and left phrenic artery 
|[[Left gastric artery]] and left phrenic artery 
|-
|-
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**Layer of [[Bicarbonate buffering system|bicarbonate ions]], secreted by the surface [[epithelial cells]].
**Layer of [[Bicarbonate buffering system|bicarbonate ions]], secreted by the surface [[epithelial cells]].
[[Image: Stomach mucosal layer labeled.svg.png|center|frame|Diagram of alkaline Mucous layer in stomach with mucosal defense mechanisms<br> '''Source''': By M•Komorniczak (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons]]
[[Image: Stomach mucosal layer labeled.svg.png|center|frame|Diagram of alkaline Mucous layer in stomach with mucosal defense mechanisms<br> '''Source''': By M•Komorniczak (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons]]
The following table demonstrates the defense mechanisms of [[gastric mucosal barrier]]<ref name="pmid3072665">{{cite journal |vauthors=Forssell H |title=Gastric mucosal defence mechanisms: a brief review |journal=Scand. J. Gastroenterol. Suppl. |volume=155 |issue= |pages=23–8 |year=1988 |pmid=3072665 |doi= |url=}}</ref>
The following table demonstrates the defense mechanisms of [[gastric mucosal barrier]]:<ref name="pmid3072665">{{cite journal |vauthors=Forssell H |title=Gastric mucosal defence mechanisms: a brief review |journal=Scand. J. Gastroenterol. Suppl. |volume=155 |issue= |pages=23–8 |year=1988 |pmid=3072665 |doi= |url=}}</ref>
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
! colspan="2" style="background:#efefef;" |Defense mechanisms of gastric mucosal barrier
! colspan="2" style="background:#efefef;" |Defense mechanisms of gastric mucosal barrier
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!Microscopic Pathology
!Microscopic Pathology
|-
|-
| colspan="2" |[[Varices]]
! colspan="2" |[[Varices]]
|Large and tortuous [[veins]] that protrude into the [[lumen]]
|Large and tortuous [[veins]] that protrude into the [[lumen]]
|Varices may be difficult to demonstrate in surgical specimens
|Varices may be difficult to demonstrate in surgical specimens
|-
|-
| colspan="2" |[[Mallory-Weiss Tear]]<ref name="pmid1465928">{{cite journal |vauthors=Renoult E, Biava MF, Aimone-Gastin I, Aouragh F, Hestin D, Kures L, Kessler M |title=Evolution and significance of Toxoplasma gondii antibody titers in kidney transplant recipients |journal=Transplant. Proc. |volume=24 |issue=6 |pages=2754–5 |year=1992 |pmid=1465928 |doi= |url=}}</ref>
! colspan="2" |[[Mallory-Weiss Tear]]<ref name="pmid1465928">{{cite journal |vauthors=Renoult E, Biava MF, Aimone-Gastin I, Aouragh F, Hestin D, Kures L, Kessler M |title=Evolution and significance of Toxoplasma gondii antibody titers in kidney transplant recipients |journal=Transplant. Proc. |volume=24 |issue=6 |pages=2754–5 |year=1992 |pmid=1465928 |doi= |url=}}</ref>
|Isolated or multiple cleft like mucosal defects
|Isolated or multiple cleft like mucosal defects
|
|
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**Epithelial regeneration
**Epithelial regeneration
|-
|-
| rowspan="5" |[[Esophagitis]]<ref name="pmid24868280">{{cite journal |vauthors=Rosołowski M, Kierzkiewicz M |title=Etiology, diagnosis and treatment of infectious esophagitis |journal=Prz Gastroenterol |volume=8 |issue=6 |pages=333–7 |year=2013 |pmid=24868280 |pmc=4027832 |doi=10.5114/pg.2013.39914 |url=}}</ref>
! rowspan="5" |[[Esophagitis]]<ref name="pmid24868280">{{cite journal |vauthors=Rosołowski M, Kierzkiewicz M |title=Etiology, diagnosis and treatment of infectious esophagitis |journal=Prz Gastroenterol |volume=8 |issue=6 |pages=333–7 |year=2013 |pmid=24868280 |pmc=4027832 |doi=10.5114/pg.2013.39914 |url=}}</ref>
|Herpes esophagitis
!Herpes esophagitis
|
|
* Shallow [[ulcers]]
* Shallow [[ulcers]]
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|Ground glass [[inclusion bodies]]
|Ground glass [[inclusion bodies]]
|-
|-
|Cytomegalovirus esophagitis
!Cytomegalovirus esophagitis
|
|
* Superficial ulcers
* Superficial ulcers
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* [[CMV]] infects mesenchymal cells in the lamina propria and submucosa
* [[CMV]] infects mesenchymal cells in the lamina propria and submucosa
|-
|-
|Fungal esophagitis
!Fungal esophagitis
|
|
* [[Erythematous]]
* [[Erythematous]]
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|[[Neutrophils]] within the squamous epithelium
|[[Neutrophils]] within the squamous epithelium
|-
|-
|Pill esophagitis
!Pill esophagitis
|
|
* Discrete ulcers
* Discrete ulcers
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* Eosinophilic infiltrate
* Eosinophilic infiltrate
|-
|-
|Toxic esophagitis
!Toxic esophagitis
|
|
* [[Erythema|Mucosal erythema]]  
* [[Erythema|Mucosal erythema]]  
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* Abundant [[granulation tissue]]
* Abundant [[granulation tissue]]
|-
|-
| colspan="2" |Gastroesophageal  
! colspan="2" |Gastroesophageal  
Reflux Disease<ref name="pmid28943113">{{cite journal |vauthors=Pandit S, Boktor M, Alexander JS, Becker F, Morris J |title=Gastroesophageal reflux disease: A clinical overview for primary care physicians |journal=Pathophysiology |volume= |issue= |pages= |year=2017 |pmid=28943113 |doi=10.1016/j.pathophys.2017.09.001 |url=}}</ref>
Reflux Disease<ref name="pmid28943113">{{cite journal |vauthors=Pandit S, Boktor M, Alexander JS, Becker F, Morris J |title=Gastroesophageal reflux disease: A clinical overview for primary care physicians |journal=Pathophysiology |volume= |issue= |pages= |year=2017 |pmid=28943113 |doi=10.1016/j.pathophys.2017.09.001 |url=}}</ref>
|
|
Line 204: Line 202:
* Squamous cell degeneration.
* Squamous cell degeneration.
|-
|-
| colspan="2" |Barrett Esophagus<ref name="pmid28501084">{{cite journal |vauthors=Rajendra S, Sharma P |title=Barrett Esophagus and Intramucosal Esophageal Adenocarcinoma |journal=Hematol. Oncol. Clin. North Am. |volume=31 |issue=3 |pages=409–426 |year=2017 |pmid=28501084 |doi=10.1016/j.hoc.2017.01.003 |url=}}</ref>
! colspan="2" |Barrett Esophagus<ref name="pmid28501084">{{cite journal |vauthors=Rajendra S, Sharma P |title=Barrett Esophagus and Intramucosal Esophageal Adenocarcinoma |journal=Hematol. Oncol. Clin. North Am. |volume=31 |issue=3 |pages=409–426 |year=2017 |pmid=28501084 |doi=10.1016/j.hoc.2017.01.003 |url=}}</ref>
|
|
* [[Erythema|Mucosal erythema]]
* [[Erythema|Mucosal erythema]]
Line 213: Line 211:
* Cells of acute [[inflammation]]
* Cells of acute [[inflammation]]
|-
|-
| colspan="2" |Acute Gastritis
! colspan="2" |Acute Gastritis
|Mucosal hyperemia associated with
|Mucosal hyperemia associated with
* [[Bleeding]]
* [[Bleeding]]
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** Adherent fibrinopurulent debris
** Adherent fibrinopurulent debris
|-
|-
| colspan="2" |Gastric Ulcers<ref name="pmid28798512">{{cite journal |vauthors=Drini M |title=Peptic ulcer disease and non-steroidal anti-inflammatory drugs |journal=Aust Prescr |volume=40 |issue=3 |pages=91–93 |year=2017 |pmid=28798512 |pmc=5478398 |doi=10.18773/austprescr.2017.037 |url=}}</ref>
! colspan="2" |Gastric Ulcers<ref name="pmid28798512">{{cite journal |vauthors=Drini M |title=Peptic ulcer disease and non-steroidal anti-inflammatory drugs |journal=Aust Prescr |volume=40 |issue=3 |pages=91–93 |year=2017 |pmid=28798512 |pmc=5478398 |doi=10.18773/austprescr.2017.037 |url=}}</ref>
|
|
* Solitary, typically less than 2 cm in diameter, and have sharply defined borders.  
* Solitary, typically less than 2 cm in diameter, and have sharply defined borders.  
Line 235: Line 233:
* Granulation tissue
* Granulation tissue
|-
|-
| colspan="2" |Portal Hypertensive Gastropathy<ref name="pmid26564121">{{cite journal |vauthors=Garg H, Gupta S, Anand AC, Broor SL |title=Portal hypertensive gastropathy and gastric antral vascular ectasia |journal=Indian J Gastroenterol |volume=34 |issue=5 |pages=351–8 |year=2015 |pmid=26564121 |doi=10.1007/s12664-015-0605-0 |url=}}</ref>
! colspan="2" |Portal Hypertensive Gastropathy<ref name="pmid26564121">{{cite journal |vauthors=Garg H, Gupta S, Anand AC, Broor SL |title=Portal hypertensive gastropathy and gastric antral vascular ectasia |journal=Indian J Gastroenterol |volume=34 |issue=5 |pages=351–8 |year=2015 |pmid=26564121 |doi=10.1007/s12664-015-0605-0 |url=}}</ref>
|
|
* Mosaic pattern of congestion
* Mosaic pattern of congestion
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* Mucosal capillaries may also show congestion, dilation, and proliferation.  
* Mucosal capillaries may also show congestion, dilation, and proliferation.  
|-
|-
| colspan="2" |Gastric Antral Vascular Ectasia<ref name="pmid26564121">{{cite journal |vauthors=Garg H, Gupta S, Anand AC, Broor SL |title=Portal hypertensive gastropathy and gastric antral vascular ectasia |journal=Indian J Gastroenterol |volume=34 |issue=5 |pages=351–8 |year=2015 |pmid=26564121 |doi=10.1007/s12664-015-0605-0 |url=}}</ref>
! colspan="2" |Gastric Antral Vascular Ectasia<ref name="pmid26564121">{{cite journal |vauthors=Garg H, Gupta S, Anand AC, Broor SL |title=Portal hypertensive gastropathy and gastric antral vascular ectasia |journal=Indian J Gastroenterol |volume=34 |issue=5 |pages=351–8 |year=2015 |pmid=26564121 |doi=10.1007/s12664-015-0605-0 |url=}}</ref>
|Linear pattern of mucosal congestion in the antrum termed “watermelon stomach
|Linear pattern of mucosal congestion in the antrum termed “watermelon stomach
|'''<u>Antral biopsies</u>''' show  
|'''<u>Antral biopsies</u>''' show  
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* Edema and regenerative changes
* Edema and regenerative changes
|-
|-
| colspan="2" |Reactive (Chemical) Gastropathy
! colspan="2" |Reactive (Chemical) Gastropathy
|
|
* [[Edema]]  
* [[Edema]]  
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* [[Hyperplasia|Foveolar hyperplasia]]
* [[Hyperplasia|Foveolar hyperplasia]]
|-
|-
| colspan="2" |Peptic Disease
! colspan="2" |Peptic Disease
|
|
* Normal/slightly edematous mucosa  
* Normal/slightly edematous mucosa  
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* The surface epithelium usually shows mucous cell (pseudopyloric) [[metaplasia]]
* The surface epithelium usually shows mucous cell (pseudopyloric) [[metaplasia]]
|-
|-
| colspan="2" |Ischemia
! colspan="2" |Ischemia
|
|
* Hypoperfused ulcers
* Hypoperfused ulcers
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* [[Strictures]]
* [[Strictures]]
|-
|-
| colspan="2" |Structural Abnormalities of Blood Vessels<ref name="pmid11355900">{{cite journal |vauthors=Gordon FH, Watkinson A, Hodgson H |title=Vascular malformations of the gastrointestinal tract |journal=Best Pract Res Clin Gastroenterol |volume=15 |issue=1 |pages=41–58 |year=2001 |pmid=11355900 |doi=10.1053/bega.2000.0155 |url=}}</ref>
! colspan="2" |Structural Abnormalities of Blood Vessels<ref name="pmid11355900">{{cite journal |vauthors=Gordon FH, Watkinson A, Hodgson H |title=Vascular malformations of the gastrointestinal tract |journal=Best Pract Res Clin Gastroenterol |volume=15 |issue=1 |pages=41–58 |year=2001 |pmid=11355900 |doi=10.1053/bega.2000.0155 |url=}}</ref>
|Large-caliber artery within the submucosa
|Large-caliber artery within the submucosa
|Dilated venules and arteriole in direct communication with each other
|Dilated venules and arteriole in direct communication with each other
|-
|-
| colspan="2" |Inflammatory Bowel Disease
! colspan="2" |Inflammatory Bowel Disease
|
|
|Lymphoplasmacytic infiltrate with numerous neutrophils
|Lymphoplasmacytic infiltrate with numerous neutrophils

Revision as of 18:57, 27 November 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

The main inciting event in the pathogenesis of upper gastrointestinal (GI) bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to ligament of Treitz, it is defined as upper GI bleeding. Regardless of etiology, if the balance of gastric acid secretion and mucosal defenses is disrupted, acid interacts with the epithelium to cause damage.

Pathophysiology

Blood Supply of Foregut

The digestive system is supplied by the celiac artery. The celiac artery is the first major branch from the abdominal aorta, and is the only major artery that supplies the digestive organs.[1][2][3][4][5][6][7]

Foregut Blood supply
Esophagus

Upper esophageal sphincter
Cervical esophagus

 Inferior thyroid artery 
Thoracic esophagus Aortic esophageal arteries or branches of the bronchial arteries 

Distal esophagus
Lower esophageal sphincter

Left gastric artery and left phrenic artery 
Stomach Lesser curvature Right and left gastric arteries
Greater curvature Right and left gastroepiploic arteries
Gastric fundus Short gastric arteries
Duodenum First and second parts

Gastroduodenal artery (GDA) and
Superior pancreaticoduodenal artery

Third and fourth parts Inferior pancreaticoduodenal artery
Blood supply of stomach
Source: By Mikael Häggström.https://commons.wikimedia.org/w/index.php?curid=3416062

Mucosal barrier

Diagram of alkaline Mucous layer in stomach with mucosal defense mechanisms
Source: By M•Komorniczak (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons

The following table demonstrates the defense mechanisms of gastric mucosal barrier:[11]

Defense mechanisms of gastric mucosal barrier
Mucus layer Forms a protective gel-like coating over the entire gastric mucosal surface
Epithelial layer Epithelial cell layer are bound by tight junctions that repel fluids
Bicarbonate ions Neutralize acids

Pathogenesis

The main inciting event in the pathogeneis of upper GI bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to ligament of Treitz, it is defined as upper GI bleeding.[12][13]

Etiology Frequency of occurance
Peptic ulcer disease 50%
Variceal bleeding 20%
Esophagitis, gastritis, and duodenitis 10-15%
Mallory-Weiss tear 15%
Malignancy 3-5%
Arteriovenous malformation <3%
Gastric antral vascular ectasia <1%
Dieulafoy lesion <1%
 
 
 
 
 
 
 
 
 
NSAIDS
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Inhibits cyclooxygenase pathway
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
COX-1
 
 
 
 
 
 
 
 
COX-2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Reduced
mucosal blood flow
 
Reduced
mucosal and
bicarbonate secreation
 
Impaired
platelet aggregation
 
Reduced
angiogenesis
 
 
 
 
Increased
leucocyte adherence
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Impaired defence
Impaired healing
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Mucosal Injury
 
 
 
 
 
 
 
 
 
 
 
 

Gross and Microscopic Pathology

Gross Pathology Microscopic Pathology
Varices Large and tortuous veins that protrude into the lumen Varices may be difficult to demonstrate in surgical specimens
Mallory-Weiss Tear[26] Isolated or multiple cleft like mucosal defects
Esophagitis[27] Herpes esophagitis Ground glass inclusion bodies
Cytomegalovirus esophagitis
  • Superficial ulcers
  • Well-circumscribed
  • CMV infects mesenchymal cells in the lamina propria and submucosa
Fungal esophagitis Neutrophils within the squamous epithelium
Pill esophagitis
  • Discrete ulcers
Not specific and include
Toxic esophagitis Acid injury

Alkaline injury

Gastroesophageal

Reflux Disease[28]

Barrett Esophagus[29] Columnar metaplasia
Acute Gastritis Mucosal hyperemia associated with
Gastric Ulcers[30]
  • Solitary, typically less than 2 cm in diameter, and have sharply defined borders.
  • The ulcer edges are usually flat, and the base of the ulcer usually appears smooth.
  • The presence of a radiating pattern of rugal folds is characteristic of peptic ulcers
  • Fibrinopurulent debris
  • Necrosis
  • Granulation tissue
Portal Hypertensive Gastropathy[31]
  • Mosaic pattern of congestion
  • Most commonly involves the fundus
  • Dilation, tortuosity, and thickening of small submucosal arteries and veins.
  • Mucosal capillaries may also show congestion, dilation, and proliferation.
Gastric Antral Vascular Ectasia[31] Linear pattern of mucosal congestion in the antrum termed “watermelon stomach Antral biopsies show
  • Congestion
  • Dilated mucosal capillaries
  • Vascular microthrombi

The mucosa also shows

  • Foveolar hyperplasia
  • Fibromuscular hyperplasia
  • Edema and regenerative changes
Reactive (Chemical) Gastropathy
  • Edema
  • Surface erosions
  • Polypoid changes, and friability
The mucosa shows
Peptic Disease
  • Normal/slightly edematous mucosa
  • Increased friability, erosions, and ulcers
Ischemia
  • Hypoperfused ulcers
Acute ischemia

Chronic ischemia

Structural Abnormalities of Blood Vessels[32] Large-caliber artery within the submucosa Dilated venules and arteriole in direct communication with each other
Inflammatory Bowel Disease Lymphoplasmacytic infiltrate with numerous neutrophils

References

  1. Feldman SE (1970). "Blood supply to stomach". Calif Med. 112 (4): 55. PMC 1501289. PMID 18730308.
  2. Granger DN, Holm L, Kvietys P (2015). "The Gastrointestinal Circulation: Physiology and Pathophysiology". Compr Physiol. 5 (3): 1541–83. doi:10.1002/cphy.c150007. PMID 26140727.
  3. Geboes K, Geboes KP, Maleux G (2001). "Vascular anatomy of the gastrointestinal tract". Best Pract Res Clin Gastroenterol. 15 (1): 1–14. doi:10.1053/bega.2000.0152. PMID 11355897.
  4. Varga F, Csáky TZ (1976). "Changes in the blood supply of the gastrointestinal tract in rats with age". Pflugers Arch. 364 (2): 129–33. PMID 986621.
  5. Matuchansky C, Bernier JJ (1973). "[Prostaglandins and the digestive tract]". Biol Gastroenterol (Paris) (in French). 6 (3): 251–68. PMID 4599528.
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