Anatomy of gastritis

2021-05-12 04:22 PM

In the mild form, the superficial epithelium remains intact and the lower layer has scattered infiltration of polymorphonuclear cells.

This is the obvious pathological entity. But the term gastritis is often overused to explain some mild or temporary symptoms such as heartburn, indigestion ... On the contrary, gastritis may not cause any clinical symptoms at all. There are 2 groups of gastritis: acute and chronic. Each group has different types.

Acute gastritis

Acute inflammation of the gastric mucosa, usually of a temporary nature, may be accompanied by bleeding in the mucosa, and possibly more severe inflammation of the mucosa.

Pathogenesis

Not known yet. Some clinical and experimental data show that the disease is often accompanied by situations such as: using non-steroidal anti-inflammatory drugs (AINS: Anti-inflammatory non-steroidal) or belonging to the long-term steroid or aspirin group, drinking a lot of alcohol, smoking a lot, drinking chemicals to treat cancer, hyperaemia, systemic infections (such as typhoid fever), staphylococcal food poisoning, severe stress (such as severe burns, trauma, surgery) , shock, radiation ... These factors can all increase acid secretion, decrease the production of buffered bicarbonate, decrease blood flow, thus causing acid stagnation and mucosal damage. stomach.

Anatomical form of the disease

Depends on the severity of the disease. Mucosa may be moderate oedema and mild congestion or sudden and bleeding. In the mild form, the superficial epithelium remains intact and the lower layer has scattered infiltration of polymorphonuclear cells. In the more severe form, called acute haemorrhagic sudden inflammation, there is a shallow sloughing of the mucosa, haemorrhage of the lower layer, and polymorphonuclear leucocytosis. There are broad areas of the mucous membrane that peel off, but these lesions are shallow, rarely affecting the full mucosal thickness and the deeper layer. Sudden inflammation is the first step to stress ulcers.

Clinical manifestations

If the illness is mild, it usually causes no symptoms. More severe, the patient may experience vomiting blood, acute abdominal pain, bloody bowel movements, vomiting, nausea. In the UK, 25% of severe illness with bowel movements and vomiting blood have been associated with aspirin or AIWS use.

Chronic gastritis

Pathogenesis

There is no clear evidence to suggest the role of pharmaceuticals, alcohol, tobacco and acute gastritis in the pathogenesis of chronic gastritis. On the other hand, long-term studies in patients with superficial chronic gastritis show that the gastric mucosa is reversible or atrophic. So superficial gastritis can be the first stage of more severe mucosal lesions.

Gastroenteritis of the fundus region: there are 2 subjects of patients:

In adults with malignant anaemia. In the group of malignant anaemia, the disease has an autoimmune cause. These patients have severe mucosal lesions such as atrophic inflammation, gastric atrophy with complete or near-complete loss of parietal cells, so there is a lack or absence of acid. There are 3 autoantibodies against parietal cells, 2 of which target IF (intrinsic factor: intrinsic factor), secreted by parietal cells that inhibit vitamin B12 uptake and induce Malignant anaemia. The third type of autoantibodies directly affects and damage parietal cells, in 80-90% of patients with malignant anaemia.

In the group of elderly patients without malignant anaemia, 60% also have autoantibodies against parietal cells but no antibodies against intrinsic factor. Some of these patients have hypochromia. It is also present in the relatives of the patients of the above group. There are no autoantibodies in these relatives. Therefore, the cause of the pathogenesis in this group of patients is still unknown.

Gastritis is the gastrointestinal area:

Has a different cause from fundus gastritis. Very few cases have autoantibodies against gastrin-secreting cells. Usually, the patient also has more peptic ulcer disease, so it is thought that the cause of both diseases is pyloric sphincter dysfunction, bile acid reflux and lysolecithin.

Anatomical form of the disease

Lesions can be present in most of the stomach, or alternating areas, or limited to the base of the stomach and body or in the cavernous cavity. Wherever it is, the injuries are the same.

In superficial inflammation, the mucous layer is flat (loss of fold) with cell and cytoplasmic permeability in the stromal layer limited to the upper third of the mucosa.

In atrophic gastritis, the mucous layer is thinner and flatter, the inflammatory cell penetrates deeper, the glands are atrophy and there are changes of the surface epithelial cells. At the base of the pharynx, there are very few parietal cells, glands are atrophy, the part that is not atrophy is stretched into the lining of mucous cells or intestinal metabolic cells. In the cavern the changes are the same as in the basal. A special feature is that, in the gastroenteritis type, the lesion can also be found in the gastrointestinal tract, while in the gastroenteritis type, the lesion is limited to the gastrointestinal tract.

In chronic gastric atrophy, the mucous folds are flat or completely lost, the mucous membrane is glossy. The atrophic glands are shortened, sometimes encompassing. The superficial epithelium and the deep concave part of the gastric mucosa have the form of mucous secretory sepulchocytes mixed with the intestinal epithelium with microvilli.

In fundusitis with malignant anaemia, parietal cells disappear almost entirely on the atrophic or remaining glands. In contrast, in gastroenteritis, parietal cells remain in the stem and at the base of the stomach. The superficial epithelium can be metamorphic or inverse.

Clinical manifestations

The disease may be asymptomatic or have acute inflammation-like symptoms including pain, epigastric discomfort, nausea, vomiting, and sometimes bleeding.

Basal atrophy is often more noticeable due to malignant anaemia and a decrease in hydrochloric acid in gastric juice.

In gastroenteritis, acid secretion is normal or low. Particularly the link: peptic ulcer disease is often accompanied by gastroenteritis (but not in the opposite direction). It is not known for sure that ulcers or inflammation existed before. But since the ulcer has healed, the inflammation will remain, so the inflammation may precede and create an ulcer.

It should be noted that both atrophic gastritis and atrophy of the stomach, whether in the cavity or the base of the stomach, are precancerous lesions. The incidence of turning into cancer was higher in the group of funditis with malignant anaemia, with the rate of 7-10% of the patients.

Hypertrophic gastritis

A rare group of diseases, with folds of the gastric mucosa, enlarged shaped like brain coils. In fact, the gastric mucosa is not enlarged but inflamed and has hyperplasia of mucous-secreting epithelial cells.

Granulomatous gastritis

The disease is rare, can occur in young patients, with sarcoid, Crohn's disease, but most often occurs alone in patients over the age of 40.

Gastritis with eosinophils

Occurs in allergic patients, patients with possible asthma. The gastric mucosa, sometimes the deeper layer, has more eosinophilia permeate. May be accompanied by granulitic or acute inflammation of the small arteries in the gastric wall.

Ulceration and the acute burst of stomach

Occurs acute, localized in the gastric mucosa after severe stress, known as stress ulcers. Other agents are aspirin, alcohol, tobacco, corticosteroid drugs, drugs of the AIWS group

Lesions are often multifocal, anywhere in the stomach, sometimes in the duodenum, in the form of superficial exfoliation or deep mucosal damage, but never deeper. If it is an ulcer, the ulcer is well-defined and is not a precursor to a chronic ulcer and does not share the same disease mechanism. The sores are usually round, less than 1 cm in diameter. The ulcer is usually dark brown due to acid infiltration and the haemorrhage is covered with red blood cells with fibrin. The ulcer base is rarely congested and is unknown because it is a shallow ulcer. The ulcer base and base are not stiff. Mucous folds remain. Depending on the duration of the disease, there may be inflammatory infiltrates at the margins and bases of the ulcers. There is no scarring or thickening of blood vessel walls.

Full recovery after the cause of the disease is gone. Full recovery takes from a few days to a few weeks.