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Acute gastritis


Gastritis is any inflammation of the gastric mucosa.

The acute gastritis is characterized by multiple superficial erosions or hemorrhagic foci in the mucosa of the stomach. Erosion is understood as a localized loss of substance, with little depth and that does not reach the muscular layer of the stomach or duodenum. When these losses of substance affect the muscle layer, it is called an acute ulcer.

These lesions of the gastric mucosa can only be diagnosed by pathological examination, therefore we must refrain from talking about gastritis to refer to nonspecific clinical manifestations such as heartburn, abdominal pain, etc. until they have been demonstrated by endoscopy.

Causes of acute gastritis

The causes that can cause acute gastritis are multiple. The most frequent are those caused by exogenous agents, mainly by acetylsalicylic acid, but also by other non-steroidal anti-inflammatory drugs and alcohol at high concentrations. The ingestion of caustics, usually accidentally, and abdominal radiation therapy can erode the mucosa and even produce ulcers.

Stress situations , caused by extensive burns, multiple trauma, or severe respiratory failure requiring assisted ventilation can also cause acute gastritis .

Patients with shock, uremia, or cirrhosis are also susceptible to erosion and bleeding of the gastric mucosa.

The mechanisms that produce ulcers vary depending on the causative agent.

When the cause is an exogenous factor, the lesions can occur either because it causes a decrease in the defenses of the stomach mucosa, or because they favor the increase in the production of gastric aggressors, such as hydrochloric acid. For example, acetylsalicylic acid works by inhibiting prostaglandin synthesis; These hormones favor the vasodilation of the arteries supplying the gastric mucosa, therefore their inhibition will result in a deficit of blood supply to the area, which favors their erosion and subsequent bleeding.

In erosions associated with septic shock, those responsible for the production of the lesions are the decrease in blood supply to the area, as well as the local release of necrotizing substances in the area.

In hypovolemic shock, the deficit of blood flow together with the production of oxygen free radicals , are the cause of the injuries.

What symptoms appear?

The symptoms of acute gastritis are nonspecific and can present as loss of appetite, nausea, burning, or abdominal pain.

They are often asymptomatic, and their first and only manifestation is gastrointestinal bleeding. This can appear as vomiting in the form of coffee grounds, which appears due to the oxidation of hemoglobin by hydrochloric acid in the stomach, or as melena, which is stool that contains digested blood and has a black, sticky appearance and odor. fetid; or even, they can produce a constant, but negligible loss of blood that translates into the appearance of anemia.

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Diagnosis of acute gastritis

As already described, the symptoms and physical examination are nonspecific, thus having little diagnostic value. However, faced with the repetition of symptoms, such as abdominal pain, nausea or burning, we must rule out the existence of gastritis by performing an endoscopy.

Endoscopy is the diagnostic method of choice, revealing diffuse or localized erosions of the gastric mucosa. These erosions may or may not be bleeding.

Performing an endoscopy can rule out other types of pathology, such as reflux esophagitis, gastric ulcer or stomach tumors.

Treatment of acute gastritis

Treatment is based on accelerating erosion healing and inhibiting bleeding, which is generally self-limited.

To accelerate the healing of the lesions, we can use two types of drugs: neutralizers of acid secretion or protectors of the gastric mucosa.

The most widely used neutralizers are antacids, hydrogen ion pump antagonists, of the cimetidine type; and proton pump inhibitors, the best known of which is omeprazole. The main drawback of these drugs is that the prolonged hypoacidity that they cause facilitates the bacterial proliferation of the stomach, and, therefore, the appearance of pneumonia when these germs pass into the respiratory tract.

The most commonly used protective drugs are sucralfate, colloidal bismuth, and prostaglandins.

To inhibit bleeding we can use drugs that reduce the blood flow of the gastric mucosa, such as vasopressin or somatostatin, or drugs that promote blood clotting at that level, such as tranexamic acid.

If the drugs are not effective in inhibiting bleeding, endoscopic treatment can be performed, by injecting sclerosing substances, which cause the vessel to block; electrocoagulation, or laser.

If all the above measures fail, we will resort to surgery.

How can I avoid it?

In many cases, the causes that produce acute gastritis are exogenous, and therefore can be prevented. For example, the administration of non-steroidal anti-inflammatory drugs should be avoided to individuals with a history of gastritis or peptic ulcer and, if their administration is necessary, we can do it together with a neutralizer of gastric secretion, such as ranitidine or omeprazole.

Similarly, neutralizers can be used prophylactically in patients who have suffered major burns, multiple trauma, shock, or in those who receive abdominal radiation therapy.

Given the non-specificity of the symptoms of acute gastritis, you should see a doctor and study any abdominal discomfort that lasts over time, especially if it involves burning, pain in the epigastrium, vomiting and, of course, digestive bleeding, whether in form of vomiting in coffee grounds or manes.


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Hello Readers, I am Nikki Bella a Psychology student. I have always been concerned about human behavior and the mental processes that lead us to act and think the way we do. My collaboration as an editor in the psychology area of ​​Well Being Pole has allowed me to investigate further and expand my knowledge in the field of mental health; I have also acquired great knowledge about physical health and well-being, two fundamental bases that are directly related and are part of all mental health.

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