Pathogenesis (development of disease)
Acute gastritis
The term acute gastritis describes a histologically (fine-tissue) confirmed inflammation of the gastric mucosa. Hyperemia (excessive blood supply to the tissue), edema (swelling or water retention), and, depending on the type of gastritis, infiltration of granulocytes (white blood cells) occur.
It is known that subsequent factors can attack or even destroy the protective gastric mucosal layer, causing acute gastritis or chronic Helicobacter pylori-negative ulcer:
- Alcohol
- Coffee (high consumption)
- Smoking
- Stress or severe life-threatening illnesses (traumatic brain injury, polytrauma, burns, patients after major surgery and long-term intubation).
- Frequent or prolonged use of so-called NSAID (non-steroidal anti-inflammatory drugs; non-steroidal anti-inflammatory drugs) increase the risk of gastroduodenal ulcer by a factor of 4: especially acetylsalicylic acid (ASS), diclofenac; glucocorticoids, cytostatic drugs, etc.
- Injuries caused by acids or alkalis
Chronic gastritis
Type A chronic gastritis (type A gastritis) often occurs in association with other autoimmune diseases, such as Hashimoto’s thyroiditis or type 1 diabetes mellitus, and antibodies to parietal cells (APCA or anti-parietal cell autoantibodies; 90% of cases) and intrinsic factor (AIF; 70% of cases) are found. Type A gastritis typically leads to pernicious anemia. Long-term complication is gastric carcinoma (stomach cancer; adenocarcinoma).Type B chronic gastritis (type B gastritis) is caused by the bacterium Helicobacter pylori. This bacterium produces an enzyme called urease in large quantities, which breaks down urea into ammonia and CO2. Since ammonia is basic, this substance is able to neutralize the acidic stomach acid. In this way, the bacterium can survive in the stomach and nests there permanently. This results in a defensive reaction of the immune system. Exactly how this leads to the destruction of the protective gastric mucosal layer has not yet been clarified. Chronic type C gastritis (type C gastritis) is triggered by the influence of toxic substances on the gastric mucosa, such as drugs – NSAIDs (non-steroidal anti-inflammatory drugs), especially acetylsalicylic acid (ASA), diclofenac; glucocorticoids, cytostatics, etc. – or by reflux (backflow) of bile and fluid from the duodenum. It is also called chemical-reactive gastritis (gastritis CR; synonyms: chemical gastritis or reactive gastritis).
Etiology (causes)
Behavioral causes
- Diet
- Irregular meal intake
- Consumption of stimulants
- Alcohol
- Coffee (high consumption)
- Smoking
- Stress
Causes related to disease
- Autoimmune diseases – e.g. Hashimoto’s thyroiditis, type 1 diabetes mellitus, Addison’s disease (primary adrenocortical insufficiency; NNR insufficiency).
- Infection with Helicobacter pylori
- Food poisoning – infections with bacteria, viruses or fungi such as Salmonella, Candida albicans.
- Crohn’s disease
- Sarcoidosis
- Syphilis
- Tuberculosis
- Injuries with acids or alkalis
- Viral infections – cytomegaly, varicella.
Medication
- Cortisone
- NSAIDs (non-steroidal anti-inflammatory drugs) – especially acetylsalicylic acid (ASA).
- Cytostatics (substances that inhibit cell growth or cell division).
X-rays
- Radiotherapy for tumor diseases
Surgeries
To prevent gastritis, routinely take an H2 receptor antagonist before surgery.
