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Pathology of Acute Gastritis

 Dr  Sampurna Roy  MD


GI Path Online- Home Page Gastric Pathology - Home Page

   
Acute gastritis is an acute mucosal inflammatory process usually of a transient nature.

Causes:

Drugs: Nonsteroidal anti- inflammatory drugs (Example: Aspirin).

Alcohol consumption.

Smoking.

Systemic infection.

Gastric irradiation.

Ischaemia.

Shock.

Stress (burn, trauma).

Uraemia.

Following surgery (distal gastrectomy)

Proposed mechanism of action:

- Increased acid production with back diffusion.           

- Decreased production of surface bicarbonate buffer.

- Reduced mucosal blood flow causing disruption of mucous layer.

- Damage to mucosal epithelium.

 

Gross:

Stress Ulcer:  Less than 1cm in diameter. Multiple lesions. Located anywhere in the stomach.
Intervening mucosa diffusely congested and numerous small petechial haemorrhages.

Acute erosive gastritis:
Mucosa is diffusely haemorrhagic without ulceration.

 

Histopathological features in acute gastritis:

Mild form:

Edema in lamina propria; Slight hyperemia in the interfoveolar area ;

Surface epithelium is intact ; Scattered neutrophils within mucosal epithelial cells - this signifies active inflammation.

Acute erosive/hemorrhagic gastritis:

-With more severe mucosal damage, erosion and hemorrhage develops.

[Erosion is defined as loss of superficial epithelium causing a defect in the mucosa that does not cross the muscularis mucosa.]

-Lesion is acccompanied  by a dense acute inflammatory infiltrate and extrusion of fibrin, containing purulent exudate into the lumen.

-Deep mucosa (glandular zone) is usually unaffected unless stress ulcer results due to local necrosis.

-Crypts may be dilated & filled with acute inflammatory cells in erosive gastritis.

Healing phase:

Epithelial regeneration ; Elongation of pit ; Pseudostratified appearance of superficial epithelium; Residual cluster of neurtrophils in the pit ; Residual cluster of neutrophils in the pit.

Note:  Pathologists should be careful not to diagnose regenerative changes as malignancy.

Regenerative changes include:

Regular glands arranged parallel to one another ;

Lamina propria separating the glands ;

Basally located nucleii ; Basophilic cytoplasm ;

Increased nuclear cytoplasmic ratio ;

Increased mitotic activity.

Summary of histological features:

-Hyperemia

-Surface erosion

-Acute inflammation

-Massive mucosal necrosis

-Sloughing

-Eventual scarring

                  

 Rare types of acute gastritis:

Suppurative gastritis:

Cause:

i) Generalized streptococcal infection 
ii) Viral infection

Gross: Distended thickened wall. Dark red in colour.
Fibrinopurulent exudate on serosal surface.
Submucosa thickened and edematous.
Mucosa is haemorrhagic and partly sloughed.

Microscopy:

Edema and acute inflammation in the submucosa with or without microabscesses.

Mucopurulent exudate may be present in the mucosa.

Mucosal sloughing.

Deep muscle congestion and necrosis.

Intravascular thrombosis in mural vessels.

Emphysematous gastritis:

Caused by gas forming organisms.
Air filled cystic space together with other features noted in suppurative gastritis.

Visit: Chronic Gastritis  ;  Autoimmune Gastritis


GI Path Online- Home Page Gastric Pathology - Home Page

 August  2015

Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)

 

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An outline of the anatomy and normal histology of the  stomach for pathologists.

Reporting of gastric biopsies (non-neoplastic gastric lesions).

Pathology and pathogenesis of peptic ulcer.   

Chronic Gastritis

Helicobacter pylori  associated (TypeB)  Gastritis 

Autoimmune Gastritis (Type A) 

Reactive /Reflux/ Chemical Gastritis (Type C)

Lymphocytic Gastritis

Collagenous Gastritis

Granulomatous Gastritis

Eosinophilic Gastritis

Gastric Xanthoma/ Xanthelasma

Other Non-Neoplastic Gastric Lesions


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