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Haemorrhagic Gastritis
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Written by Dr Sebastian Zeki
MCQs for this page
Haemorrhagic Gastritis
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Acute hemorrhagic erosive gastropathy
The hallmark of acute
hemorrhagic and erosive
gastropathy is the develop
-
ment of hemorrhagic and
erosive lesions
Mechanisms of Injury:
The normal protective barrier (which includes secreted mucins, bicarbonate, and the
epithelium itself) is disrupted.
An additional specific pathogenetic factor in NSAID-induced acute hemorrhagic and
erosive gastropathy is the inhibition of prostaglandin production.
Acid
Bile acids
Proteases
Factors Damaging the Surface
epithelium:
NSAIDs.
Alcohol.
Bile acids.
Mucosal hypoxia(burns, trauma, sepsis).
Chemotherapy.
Stress-related lesions (Curling's
ulcers): Ulcers are: Multiple
Shallow
Measure 0.5 to 2.0 cm in diameter
Almost exclusively located in the
corpus and fundus.
Histology:
Erosions may have only subtle features
eg. thin, regenerative epithelium
provides the only evidence for their
occurrence.Inflammation is usually
slight (consisting of no more than a few
neutrophils) or absent.
Treatment and prevention:
Discontinuation of the offending agent.
Antisecretory therapy-often used to limit concomitant damage from acid exposure.
Prophylaxis- eg antisecretory sometimes used to prevent stress ulceration in the
intensive care unit , and for those undergoing chemotherapy.
Acute haemorrhagic and Erosive Gastropathy
This permits acid and other luminal substances (eg. proteases and bile acids) to
penetrate into the lamina propria, where they cause additional injury to the vasculature,
stimulate nerves, and cause the release of histamine and other inflammatory mediators
Written by Dr Sebastian Zeki
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