ACUTE GASTRITIS

what is acute gastritis?

• Transient mucosal inflammatory process.
• Asymptomatic to symptoms like epigastric pain, nausea ,vomiting.
• Complicated to erosions,ulceration,hematoma,malena(blood stained stools)hemorrhage and also massive chronic blood loss 

normal histology of stomach:

Pathogenesis:
        The gastric lumen is highly acidic and it helps in digestion yet it can also cause damage to the mucosa .The mucosal damge is protected by lots of mechanisms . Some are

• Mucin secreted by foveolar cells.
• Mucus forms an unstirred layer of fluid over the epihtelium and also forms a neutral pH.
• The rich vascular supply provides oxygen and nutrients and also washes away the acid the has back diffused into the lamina propria of the layer. 

Acute or Chronic gastritis can be caused by the following mechanisms

• Reduced synthesis of mucin.
• NSAID's through reduced secretion of prostaglandins.
• Through secretion of urease by the helicobacter pylori infection.
• Ingestion of harsh chemicals like acid as a suicidal attempt or accidentally.
• Direct cellular injury through drugs chemotherpy ,alcohol,etc..including those which are mitotic inhibitors.
• Those substances which cause decreased oxygen supply.

Morphology:

The fiure shows the neutrophilic infiltretes during the acute inflammation process

•  Lamina propria shows only mild edema and vascular congestion .
• THE SURFACE EPITHELIUM IS INTACT.
• These both occur in mild acute gastritis.
• If the neutrophils and lymphocytes are present in large numbers above the basement membrane in contact with the epithelial cell. then it indicates ACTIVE INFLAMMATION.
• Complicated to erosions* and hemorrhage*.
• Concurrent erosion and hemorrhage leads to ACUTE EROSIVE HEMORRHAGIC GASTRITIS.
• It should be superficial if it extends deep then it leads to ulceration.

*erosion:loss of superficial epithelium with a defect in the mucosa limited to the lamina propria.neutrophil infiltrate within the mucosa and fibrin containing purulent exudate in the lumen .
*hemorrhage:they cause dark punctae and lead to hyperemic mucosa.


Acute gastric ulceration: what is it?

It usually occurs after NSAID's and severe physiological stress .and so differnt names are given to it . they are :

• Stress ulcers with shock and severe trauma.
• Curling ulcers in the proximal duodenum associated with burns or trauma .
• Cushing ulcers with intracranial disease and they carry a high risk of perforation.

Pathogenesis?

• Associated with NSAID's: due to inhibition of cyclooxygenase ->which prvents the production of prostaglandins->prevents the production of mucus -> ersion of the layer and on the long run it causes ulcer .
• Association with intracranial injury: direct vagal stimulation-> hypersecretion of the acid.
• Systemic acidosis.
• Hypoxia and educed blood flow.

Morphology:

• Shallow lesions to deeper erosions.
• They are round and the base is usually brown to black .This is due to the acid digestionof the extravasated blood and causes transmural inflammation and local serositis.
• Found anywhere in the stomach.
• Mutiple ulcers occur.
• They are sharply demarcated .
• Duration of the ulceration is the dependence factor.
• Scarring and thickening of the blood vessels are absent .
• Healing by re-epithelialisation occurs soon after the factors are removed . It takes weeks to months to heal.

Clinical features :

• Bleeding from superficial gastric erosions or ulcers. They may require transfusion.
• Perforation can occur.

        Treatment:

• Prophylactic H2 receptor antagonists(rantidine, cemetidine).
• Proton pump inhibitors(omeprazole).