GASTRITIS

What is Gastritis? 

Definition: The term gastritis should be reserved for histologically documented inflammation of the gastric mucosa.

Gastritis is not the mucosal erythema seen during endoscopy and is not interchangeable with “dyspepsia.” 

The etiologic factors leading to gastritis are broad and heterogeneous. 

Gastritis has been classified based on time course (acute vs chronic), 

There is no typical clinical manifestation of gastritis.

Classification Of Gastritis

1, Acute gastritis

   a. Acute H. pylori infection

   b. Other acute Infectious gastritides

       1. Bacterial (other than H. pylori)

       2. H. heilmannii

       3. Phlegmonous

       4. Mycobacterial

       5. Syphilitic

       6. Viral

       7. Parasitic

       8. Fungal

The most common causes of acute gastritis are infectious.

Acute infection with H. pylori induces gastritis. It is reported as presenting with sudden onset of epigastric pain, nausea, and vomiting, and limited mucosal. histologic studies demonstrate a marked infiltrate of neutrophils with edema and hyperemia.

If not treated, this picture will evolve into one of chronic gastritis.

Potential iatrogenic causes include polypectomy and mucosal injection with India ink. Organisms associated with this entity include streptococci, staphylococci, Escherichia coli, Proteus, and Haemophilus species.

TREATMENT: Failure of supportive measures and antibiotics may result in gastrostomy.

B. Chronic atrophic gastritis

Chronic gastritis is identified histologically by an inflammatory cell infiltrate consisting primarily of lymphocytes and plasma cells, with very scant neutrophil involvement.

Chronic gastritis has been classified according to histologic characteristics. These include superficial atrophic changes and gastric atrophy.

Type A: Autoimmune, body-predominant

Type B: H. pylori–related, antral-predominant

      

The early phase of chronic gastritis is superficial gastritis. The inflammatory changes are limited to the lamina propria of the surface mucosa, with edema and cellular infiltrates separating intact gastric glands. 

The next stage is atrophic gastritis. The inflammatory infiltrate extends deeper into the mucosa, with progressive distortion and destruction of the glands. 

The final stage of chronic gastritis is gastric atrophy. Glandular structures are lost, and there is a paucity of inflammatory infiltrates. Endoscopically, the mucosa may be substantially thin, permitting clear visualization of the underlying blood vessels. Intestinal metaplasia is an important predisposing factor for gastric cancer.

TREATMENT:Chronic Gastritis

Treatment in chronic gastritis is aimed at the sequelae and not the underlying inflammation.

 Patients with pernicious anemia will require parenteral vitamin B12 supplementation on a long-term basis. 

Eradication of H. pylori is often recommended even if PUD or a low-grade MALT lymphoma is not present.