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Gastric Ulceration - Horse (view source)

Revision as of 20:55, 30 July 2010

1,627 bytes removed ,  20:55, 30 July 2010
→‎Intrinsic protective factors
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*'''Mucus:''' secreted by specialised mucous neck cells.  A viscous, hydrophobic glycoproteinaceous gel that adheres to the mucosa and resists acid and pepsin contact. Also acts as a lubricant to minimise mechanical damage.(EGUC)
 
*'''Mucus:''' secreted by specialised mucous neck cells.  A viscous, hydrophobic glycoproteinaceous gel that adheres to the mucosa and resists acid and pepsin contact. Also acts as a lubricant to minimise mechanical damage.(EGUC)
 
*'''Bicarbonate:''' secreted by gastric mucosal cells.  Secretion triggered by luminal acid concentrations, mechanical irritation, and release of endogenous prostaglandins. Bicarbonate trapped in the mucous layer forms a pH gradient allowing a physiological pH at the mucosal surface and a gastric acid pH at the luminal surface.(EGUC)
 
*'''Bicarbonate:''' secreted by gastric mucosal cells.  Secretion triggered by luminal acid concentrations, mechanical irritation, and release of endogenous prostaglandins. Bicarbonate trapped in the mucous layer forms a pH gradient allowing a physiological pH at the mucosal surface and a gastric acid pH at the luminal surface.(EGUC)
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*'''Epidermal growth factors:''' found in salivary gland secretions, promote DNA synthesis and proliferation of gastric mucosal cells. Also play a role in prostaglandin synthesis. PGE2 is involved in:
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*'''Epidermal growth factors:''' found in salivary gland secretions, promote DNA synthesis and proliferation of gastric mucosal cells. Also play a role in prostaglandin synthesis and inhibit HCl secretion by the parietal glands.(EGUC)
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Suppression of HC1 secretion  
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*'''Epithelial restitution mechanisms:''' important in the maintenance of gastric mucosal integrity (maintain tight junctions). Epithelial injury induces migration of adjacent cells to replace damaged cells within minutes without the need of new cell proliferation.  Shear forces, induced by mixing of ingested material, are counteracted by epithlial restoration.(EGUC)
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*'''Adequate mucosal blood supply:''' required to provide the mucosa with oxygen and nutrients to produce the mucus-bicarbonate layer and to support rapid turnover of epithelial cells.  Also required to remove acid that has diffused through the mucous layer to the mucosa.(EGUC)
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*'''Prostaglandins:''' inhibit acid secretion, promote mucosal blood flow (through vasodilation), increase mucus and bicarbonate secretions and support mucosal cell repair.  PGE2 is especially important in these functions.(EGUC)
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=====Squamous mucosal defence mechanisms=====
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*'''Intercellular tight junctions''' and '''intracellular buffering systems''' act as barriers
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*'''Epidermal growth factor''' has also been found to contribute to the healthy maintenance and repair of gastric squamous epithelium (Jeffrey et al. 200 in(Martineau 2009)
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*'''Leukotrienes''' provide mucosal protection
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The squamous mucosa has limited defences.  Once these have been penetrated by acid, acid accumulation leads to necrosis and ultimately ulceration.(EGUC)
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Epithelial restitution mechanisms (maintain tight junctions) Epithelial cell restitution is another important mechanism in the maintenance of gastric mucosal integrity. Epithelial cells act as a protective covering, counter shear forces that induce damage, and provide rapid restoration of damaged protective barriers. In the case of the gastric mucosa, epithelial injury induces a migration of adjacent cells to replace damaged cells. This occurs within minutes without need of new cell proliferation. Shear forces, induced by mixing of ingested material raking against the mucosal wall, cause cell damage that is normally countered by the process of epithelial restoration.
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=====Other intrinsic defence mechanisms=====
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Adequate mucosal blood supply. An abundant mucosal blood supply is required to provide the mucosa with the oxygen and nutrients necessary to produce the mucus-bicarbonate layer and to support the rapid turnover of epithelial cells. An adequate blood supply is also required to remove acid that has diffused through the mucous layer to the mucosa. Alterations in blood flow (i.e., shock, microvascular thrombosis) are highly correlated with mucosal erosions and gastric ulcers in man. Epidermal growth factors are found in salivary gland secretions and promote DNA synthesis and proliferation of gastric mucosal cells. They also play a role in prostaglandin synthesis and inhibit the parietal gland secretions of hydrochloric acid.
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'''Gastrodudodenal motility'''
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Prostaglandins have an important role in gastric mucosal protection, although their precise mechanism is vague. Prostaglandins inhibit acid secretion, promote mucosal blood flow (vasodilate), increase mucus and bicarbonate secretions, and support mucosal cell repair.
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In the nonglandular region, intercellular tight junctions and intracellular buffering systems act as barriers, while the  Adequate mucosal blood flow and mucus secretion is maintained by appropriate prostaglandin release (Morrissey et al. 2008).  Epidermal growth factor has also been found to contribute to the healthy maintenance and repair of equine gastric squamous epithelium (Jeffrey et al. 2001). (Martineau 2009) Gastrodudodenal motility.
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Squamous mucosal defence mechanisms
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Many discussions surrounding equine squamous disease are extrapolated from human oesophageal disease and data from other species. In these species, the initial response of squamous tissues exposed to acid is to thicken.
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Cell-to-cell junctions are closely adhered (‘tight junctions’), which ensures a weak acid barrier. Buffering also is a component of the squamous tissue defence scheme, but unlike the glandular portion, there is no external mucus-bicarbonate layer. Rather, squamous tissues buffer internally (within the cell) and use leucotrienes for defence. By contrast, glandular tissue relies on prostaglandins for adequate mucosal protection.
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In summary, the squamous tissues of the stomach have a limited number of defence mechanisms that centre around acid repulsion and intracellular buffering. Once the acid penetrates these defences, it builds up within the cell layers and necrosis (cell death) leads to ulcer formation.
      
==Risk Factors==
 
==Risk Factors==
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