Etiology and pathogenesis
The disease rarely occurs out of nowhere. It may develop as an idiopathic condition, but much more often it is a direct consequence of specific triggers.
The main etiological factors are divided into several groups:
- Alimentary and infectious. Consumption of coarse or substandard food, as well as foodborne toxicoinfections (primarily caused by staphylococci and salmonellae).
- Drug-induced injuries. Non-steroidal anti-inflammatory drugs (such as acetylsalicylic acid) are the leaders here. Their damaging effect is associated not only with direct contact but also with a systemic mechanism: the drugs inhibit the synthesis of prostaglandins, which are a crucial factor in mucosal protection. The outcome of such exposure is often the development of acute erosive gastritis.
- Toxic and allergic agents. This group includes the effects of alcohol and manifestations of food allergies.
- Stress and endogenous factors. They lead to the development of so-called secondary gastritis. These include severe systemic stresses (extensive surgeries, severe trauma, burns), pronounced organ failure (hepatic, renal, respiratory), as well as hemodynamic disorders (e.g., against the background of congestive heart failure).
Clinical and diagnostic forms
Depending on the depth of the lesion and the clinical picture, two key forms of the disease are distinguished.
Acute catarrhal gastritis
This is the classic variant of inflammation. After contact with the damaging factor, a latent period occurs, usually lasting from 6 to 8 hours. Then a characteristic clinical picture unfolds:
- Pain syndrome: localized predominantly in the epigastric region.
- Dyspeptic disorders: pronounced nausea and vomiting. Admixtures of mucus and bile may be visually determined in the vomit.
- General symptoms: a systemic inflammatory response may manifest as subfebrile body temperature.
- Endoscopic picture: during esophagogastroduodenoscopy (EGD), the physician reveals a pattern of diffuse hyperemia of the gastric mucosa.
Acute erosive gastritis
This form is considered the most dangerous due to the high risk of fatal complications, primarily gastrointestinal bleeding. The insidious nature of the erosive lesion lies in its clinical presentation:
- Symptoms are often mild or masked: the patient complains only of mild pain, minor discomfort, or moderate nausea.
- On objective examination, abdominal palpation reveals tenderness in the epigastric region.
- Diagnostics: routine plain radiography of the stomach in this situation is completely uninformative. The main and only reliable diagnostic method is EGD. The endoscopist visualizes multiple erosions located against the background of a hyperemic mucosa.
Principles of treatment
Therapeutic tactics for acute gastric injury are based on two pillars: eliminating the cause and protecting the damaged mucosa.
- Elimination of the etiological factor. This is the first and most important step. If drugs (NSAIDs) were the trigger, their immediate withdrawal is required.
- Treatment of the underlying disease. In secondary gastritis, it is necessary to relieve the condition that caused the erosions. Treatment of congestive heart failure, burn disease, and correction of organ dysfunction are carried out.
- Symptomatic therapy. Aimed at alleviating the patient's condition. It includes adequate pain management, and in the event of the main complication of the erosive form (gastrointestinal bleeding), emergency replacement of blood loss.
- Diet therapy. A strict sparing anti-ulcer diet is prescribed, excluding any thermal, chemical, and mechanical irritants.
- Medication support. If necessary, drugs that reduce gastric acidity are included in the treatment regimen to decrease the aggressive impact of acid on inflamed or eroded areas.
Briefly: answers to topical questions
What clinical and morphological forms of acute gastritis exist besides catarrhal and erosive?
In addition to catarrhal and erosive, fibrinous, purulent, necrotic, hemorrhagic, and emphysematous variants of acute inflammation of the mucous membrane are distinguished.
- Fibrinous — a form distinguished depending on the depth and nature of the damage.
- Purulent (Phlegmonous gastritis) — acute panmural infectious gastritis caused by non-gas-forming microorganisms.
- Necrotic — corrosive gastritis occurring upon ingestion of alcohol surrogates and chemical burns.
- Hemorrhagic — an independent morphological form of inflammation.
- Emphysematous (Emphysematous gastritis) — a process caused by acute infection with gas-forming microorganisms.
What specific groups of pharmacological drugs are used to reduce acidity in the treatment of gastritis?
To reduce acidity and provide antisecretory therapy for gastritis, proton pump inhibitors and antacids are indicated in the sources.
- Proton pump inhibitors — baseline antisecretory therapy for erosive gastritis and duodenitis, including those associated with NSAID use; examples: omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole.
- Antacids — used in acute gastritis along with diet and sorbents.
Class and exam questions
What is the fundamental difference between acute and chronic gastritis at the microscopic level?
In acute gastritis, acute inflammatory changes predominate in the mucous membrane. In a chronic course, inflammation recedes into the background, while structural remodeling (dysregeneration) and progressive tissue atrophy leading to impaired gastric function dominate.
Why is radiography not prescribed when erosive gastritis is suspected?
Because radiography is uninformative for detecting superficial mucosal damage (erosions). Direct visual examination — EGD — is necessary for accurate diagnosis.
How exactly do aspirin and other NSAIDs lead to the development of erosions?
These drugs inhibit the synthesis of prostaglandins in the body. Since prostaglandins act as a crucial protective factor for the gastric mucosa, their deficiency leaves the organ wall defenseless against acid, leading to inflammation and erosion formation.
What else to study on this topic
- Mechanisms of dysregeneration and atrophy during the transition of acute inflammation to chronic
- Pathogenesis of stress erosions in severe systemic pathologies (burns, multiple organ failure)
- Groups of drugs to reduce gastric juice acidity and their mechanisms of action
- Differential diagnosis of causes of gastrointestinal bleeding
- Features of the principles of sparing anti-ulcer diet therapy
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