Pathogenesis of type C gastritis. Pathophysiology. Chronic gastritis


The most common are gastritis, peptic ulcer and cancer.


Gastritis of the stomach gastritis. In acute gastritis, inflammation can cover the entire stomach (diffuse gastritis) or certain parts of it (focal gastritis). The latter is divided into fundic, antral, pyloroanthral and pilo-rhoduodenal gastritis. Depending on the characteristics of morphological changes in the gastric mucosa, the following forms of acute gastritis are distinguished:


1) catarrhal, or simple;


2) fibrinous;


3) purulent (phlegmous);


4) necrotic.


Chronic gastritis can be autoimmune (type A gastritis) or non-immune (type B gastritis). With autoimmune gastritis, the formation of antibodies to parietal cells occurs, so the fundus is more often affected. In connection with the defeat of the parietal cells, the production of hydrochloric acid is reduced. With non-immune gastritis, the antrum is affected and the production of hydrochloric acid is moderately reduced. Topographically, antral, fundal and pangastritis are distinguished. Chronic gastritis is characterized by long-term dystrophic and necrobiotic changes in the mucosal epithelium, resulting in a violation of its regeneration and structural restructuring of the mucosa.


Peptic ulcer is a chronic relapsing disease, morphologically expressed by the formation of gastric or duodenal ulcers. According to localization, ulcers located in the pyloroduodenal zone or the body of the stomach are distinguished, although there are also combined forms.


The reasons for the formation of ulcers are different: the infectious process, allergic, toxic and stress factors, drug and endocrine factors, as well as postoperative complications (peptic ulcers). It is important to note the presence of predisposing factors - this is senile age, male sex, first blood type, etc.


During the formation of an ulcer, an important role is played by erosion, which is a defect in the mucous membrane that does not penetrate beyond the muscle layer. Erosion is formed as a result of necrosis of the mucous membrane area, followed by hemorrhage and rejection of dead tissue.


An acute ulcer has an irregular round or oval shape and resembles a funnel. As the necrotic masses are cleared, the bottom of the acute ulcer, represented by the muscular layer, is revealed. The bottom is painted (due to hematin) in a dirty gray or black color.


There is a period of remission and exacerbation. During the period of remission, there is scar tissue at the edges of the ulcer, the mucous membrane along the edges is thickened and hyperemic. During the period of exacerbation, a wide zone of fibrinoid necrosis appears in the area of ​​the bottom and edges of the ulcer. Fibrinous-purulent or purulent exudate is located on the surface of necrotic masses.



  • Diseases stomach: gastritis, ulcerative disease. Most common gastritis, ulcerative disease and cancer. Gastritis is an inflammation of the mucous membrane stomach.


  • Diseases stomach: gastritis, ulcerative disease. Most common gastritis, ulcerative disease and cancer. Gastritis is an inflammation of the mucous membrane stomach.


  • Most common gastritis, ulcerative disease and cancer. Gastritis is an inflammation of the mucous membrane stomach. Distinguish between acute and chronic gastritis.


  • Most common gastritis, ulcerative disease and cancer. Gastritis is an inflammation of the mucous membrane stomach. Distinguish between acute and chronic gastritis.


  • Diseases stomach: gastritis, ulcerative disease. Most common gastritis, ulcerative disease and cancer. Gastritis is an inflammation of the mucous membrane stomach.


  • “Previous question. Diseases stomach: gastritis, ulcerative disease.
    It is enough to download cheat sheets on internal diseases- and you are not afraid of any exam!


  • Diseases stomach: gastritis, ulcerative disease.
    stomach


  • Diseases stomach: gastritis, ulcerative disease.
    There is the following classification of cancer stomach. 1. By localization, they distinguish: pyloric, less curvature of the body with a transition to the walls, cardiac, greater curvature, fundic and total.


  • Diseases stomach: gastritis, ulcerative disease.
    There is the following classification of cancer stomach. 1. By localization, they distinguish: pyloric, less curvature of the body with a transition to the walls, cardiac, greater curvature, fundic and total.


  • Diseases stomach: gastritis, ulcerative disease.
    There is the following classification of cancer stomach. 1. By localization, they distinguish: pyloric, less curvature of the body with a transition to the walls, cardiac, greater curvature, fundic and total.

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GASTRITIS is a lesion of the gastric mucosa with predominantly inflammatory changes in the acute development of the process with progressive atrophy of the mucosa in a chronic course.

Etiology:

Classification:

Type A (autoimmune);

Type B (bacterial);

Type C (reactive or chemical)

Symptoms:

Pain syndrome - in the epigastric region, moderate activity

Dyspeptic syndrome

1. Belching:

acidic (with normal and increased secretion);

rotten (with reduced secretion)

2. Nausea, vomiting

3. Decreased appetite

4. Flatulence

5. Rumbling

6. Unstable Chair:

Tendency to constipation (with normal and increased secretion);

Tendency to diarrhea (with reduced secretion)

7. Dumping syndrome (with reduced secretion) - after eating:

weakness;

sweating;

dizziness;

heartbeat

Gastrointestinal bleeding (with erosive gastritis)

1. Vomiting "coffee grounds"

Diagnostics:

Mucosal biopsy (to detect Helicobacter pylori);

pH-metry;

Study of the level of gastrin

1. easily digestible diet;

2. exclusion of alcohol and NSAIDs;

3. eradication therapy;

4. gastroprotectors

Ticket 3

1. The concept of "symptom", "syndrome", "symptom complex". Classification of symptoms (pathognomonic, specific, non-specific; explicit, hidden; subjective and objective), examples.

A symptom is a statistically significant deviation of one or another indicator from the norm or the appearance of a qualitatively new phenomenon that is not characteristic of a healthy organism.

A syndrome is a persistently observed combination of symptoms united by a single pathogenesis.

Symptom complex - a group of symptoms or syndromes characteristic of a particular disease, but not united by a common origin.

Classification.

Pathognomonic symptoms are characteristic of strictly defined diseases, and do not occur in any other. For example: "mitral" in stenosis of the left AV foramen, megaloblasts and rudiments of nuclei in erythrocytes in vitamin B12-deficient anemia, mononuclear cells in infectious mononucleosis, plasmodia in malaria)

Specific symptoms are characteristic changes in the body affected by the main pathological process, but they are also found in other diseases of this organ. For example: ulcer yavl. a specific symptom of peptic ulcer disease, but can be observed in stomach cancer and other diseases.

Nonspecific symptoms are found in a variety of diseases and occur as a result of functional disorders of the nervous and cardiovascular systems: general weakness, malaise, fatigue, sleep disturbance, appetite.



Explicit symptoms - are determined by direct examination.

Latent symptoms - are determined when performing special tests or laboratory - instrumental research.

Subjective symptoms - sensations of the patient (complaints).

Objective symptoms - changes detected by a doctor (physical or additional methods).

2. Nephrotic and nephritic syndromes. Definition. Symptomatology. Laboratory and instrumental diagnostics. clinical significance.

NEPHROTIC SYNDROME

Clinical and laboratory criteria:

Anasarca, edema, proteinuria, ischemic heart disease

NEPHROTIC SYNDROME



Nephrotic syndrome is more common in children and adults under 35 years of age, but can also develop in old age.

The reason for the development of massive proteinuria in nephrotic syndrome is damage to the wall of the renal glomerulus with an increase in its permeability to plasma proteins and a decrease in protein reabsorption in the tubules. Morphological variants of kidney damage in nephrotic syndrome:

Minimal basement membrane changes;

Focal segmental glomerulosclerosis;

membranous glomerulonephritis;

Mesangioproliferative glomerulonephritis;

Mesangiocapillary glomerulonephritis;

Diabetic glomerulosclerosis;

Amyloidosis.

Despite various variants of kidney damage leading to the development of nephrotic syndrome, its clinical and laboratory manifestations are nonspecific. Diagnostic criteria for nephrotic syndrome are:

Proteinuria > 3.5 g/day;

Hypoalbuminemia (albumin< 30 г/л) и диспротеинемия;

Massive swelling;

Dyslipidemia.

Reasons for the development of edema in nephrotic syndrome:

Hypoproteinemia and a decrease in plasma oncotic pressure leads to hypovolemia and activation of the renin-angiotensin-aldosterone system and ADH (antidiuretic hormone), resulting in increased reabsorption of sodium and water by the kidneys;

With normo- and hypervolemia (60-70% of patients) and the absence of high activity of the "renin-angiotensin-aldosterone" system, the development of edema is explained primarily by renal sodium retention;

The BCC value determines the tactics of prescribing diuretics in patients with nephrotic syndrome.

Clarification of the cause of the development of nephrotic syndrome is important for the choice of treatment tactics.

When examining a patient with nephrotic syndrome, it is necessary first of all to exclude the paraneoplastic genesis of the disease, diabetic nephropathy and amyloid damage.

kidneys (biopsy of the kidney, rectal mucosa, gums), since in these cases immunosuppressive therapy is not indicated. To clarify the diagnosis, an immunological examination is performed (NS may develop as part of a systemic disease) and, if possible, a kidney biopsy; Treatment is as follows:

Antibacterial therapy for infection (infective endocarditis);

Removal of the focus of suppuration or tumor;

Deciding on the appointment of pathogenetic therapy (glucocorticosteroids and / or cytostatics).

Renal protective therapy (ACE inhibitors, statins, anticoagulants and antiaggregants).

A long-term nephrotic syndrome, regardless of its cause, leads to the development of chronic renal failure, the risk of progression of renal failure is higher, the higher the proteinuria.

1. Pathophysiology of chronic H. pylori gastritis and the natural history of H. pylori infection

H. pylori infection is characterized by long-term persistence on the gastric mucosa with the development of infiltration of its own plate by inflammatory cells. Infection with H. pylori always leads to the development of an immune response, which almost never ends, however, in the complete elimination of the pathogen. First of all, this is due to the fact that, unlike other extracellular pathogens, H. pylori causes an immune response of the predominant first type, accompanied by activation of the cellular link of immunity.

The development of neutrophilic infiltration of the lamina propria is associated with two different mechanisms. The direct mechanism is realized through the release of the H. pylori neutrophil-activating protein, and the indirect one is through the stimulation of IL-8 expression by epithelial cells, followed by the launch of a complex inflammatory cascade.

Migrating into the gastric mucosa, granulocytes, by releasing reactive oxygen species, damage epithelial cells and intensively produce pro-inflammatory cytokines. Under such conditions, against the background of the progression of inflammation, in some cases, damage and death of epithelial cells with the formation of erosive and ulcerative defects occur, while in others atrophy, metaplasia and neoplasia of the gastric mucosa gradually form.

Another significant feature of the pathogenesis of H. pylori infection is the failure of humoral immunity and the lack of eradication under the influence of anti-Helicobacter antibodies. This fact is usually explained by the "inaccessibility" of the bacterium for antibodies in the layer of gastric mucus, the impossibility of isolating IgG into the gastric lumen with a relative deficiency of secretory IgA, as well as "antigenic mimicry" of the bacterium.

Despite the fact that chronic gastritis develops in all people infected with H. pylori, there are not any clinical manifestations in every case. In general, for H. pylori-positive patients, the lifetime risk of developing peptic ulcer and gastric cancer is 10-20% and 1-2%, respectively.

Duodenal ulcer (DU) and gastric cancer are commonly associated with different types of chronic gastritis. With antral gastritis with no or minimal atrophy, normal or increased secretion of hydrochloric acid, duodenal ulcers often develop. With pangastritis with severe atrophy of the mucous membrane, hypo- or achlorhydria, gastric cancer is much more often recorded.

This fact was explained after the discovery of H. pylori, when it became clear that in most cases antral gastritis and pangastritis represent different directions of the natural course of this infection.

After infection, which usually occurs during childhood or adolescence, H. pylori causes acute gastritis with nonspecific transient symptoms of dyspepsia (pain and heaviness in the epigastrium, nausea, vomiting) and hypochlorhydria.

In the future, acute Helicobacter pylori gastritis becomes chronic. Gradually, either superficial antral gastritis or atrophic multifocal pangastritis is formed. The key factor determining the topography of gastritis, and hence the likelihood of developing duodenal ulcer or gastric cancer, is the level of secretion of hydrochloric acid.

In individuals with normal or high secretory activity of parietal cells, hydrochloric acid inhibits the growth of H. pylori in the body of the stomach, and the bacterium intensively colonizes only the antrum, causing, accordingly, limited antral gastritis. Chronic inflammation in the antrum leads to hypergastrinemia and hyperchlorhydria, acidification of the duodenal cavity and ulceration. In patients with a reduced level of hydrochloric acid secretion, H. pylori freely colonizes the mucous membrane of the body of the stomach, causing pangastritis. Chronic active inflammation, through the effects of a number of cytokines, further inhibits the function of parietal cells, and further causes the development of atrophy and metaplasia of the major glands. As a result, this category of patients significantly increases the risk of developing stomach cancer.

According to modern concepts, the determining role in the determination of these processes belongs to the genetic factors of the human body. They are directly related to the features of the immune response, in particular, the level of production of the pro-inflammatory cytokine IL-1b, which has pronounced antisecretory properties. Genetically determined overexpression of this substance causes persistent suppression of hydrochloric acid secretion already at the stage of acute H. pylori gastritis. In this situation, favorable conditions are created for the settlement of H. pylori in the body of the stomach.

The close relationship between gastric cancer and H. pylori has also been confirmed by large epidemiological studies. The presence of infection increases the risk of developing this malignant tumor by 4-6 times. Patients with H. pylori-associated chronic atrophic pangastritis are even more likely to develop neoplasia. The International Agency for Research on Cancer has classified H. pylori as a class I human carcinogen for non-cardiac gastric cancer.

Thus, chronic Helicobacter pylori gastritis is the background against which, in most cases, gastric cancer develops. An important condition for its occurrence is the presence of violations of cell renewal in the gastric mucosa in the form of its atrophy and intestinal metaplasia.

adenovirus infection

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Gastritis

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Diagnosis of chronic gastritis

Diagnosis of chronic gastritis includes the following steps: history taking and external examination, physical examination, endoscopic diagnosis (gastroscopy), laboratory tests of blood and gastric juice...

Diagnosis of chronic gastritis

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Diagnosis of chronic gastritis

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Cardiac ischemia

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Cardiomyopathy and myocarditis

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Acute and chronic gastritis

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Acute and chronic gastritis

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Parenteral hepatitis and HIV infections

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Chronic gastritis

A reliable diagnosis of chronic gastritis can only be established after a morphological study of biopsy specimens of the gastric mucosa by a morphologist ...

Chronic gastritis

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Gastritis is a long-term disease that manifests itself in changes in the mucous membrane of an inflammatory, and often dystrophic nature. It causes a violation of the regeneration and atrophy of epithelial cells, as well as the replacement of healthy glands with fibrous tissue.

But what is atrophic gastritis? What are its symptoms, causes, how to treat it, what could be the consequences? That is what we are going to talk about now.

Characteristics of the disease and etiology

Before proceeding to consider the symptoms of atrophic gastritis, it is worth talking about what it is in general.

So, this is one of the most dangerous forms of the disease in question. It is diagnosed in the event that a person has inflammatory processes in the pancreas and in the mucous membrane. Also, during the course of this disease, the cells that are responsible for the production of gastric juice cease to function normally. Because of this, the glands that produce hydrochloric acid and enzymes subsequently die.

Atrophic gastritis often spreads to the entire stomach as a whole, and not just to part of the organ. Also, it is this disease that often causes a precancerous condition.

The reasons why this disease occurs include the following:

  • Lack of a balanced and rationed diet.
  • Addiction to alcoholic beverages.
  • Mental and nervous strain.
  • Smoking.
  • Violations of the endocrine system.
  • hereditary predisposition.

Any of the above first leads to a violation of the integrity of the mucous membrane, and the result of this is its inflammation. Then the disease begins to develop rapidly.

signs

The main symptom of focal atrophic gastritis is the formation of local inflammation in the wall of the stomach, accompanied by an increase in the function of its healthy areas (compensation mechanism).

But these changes cannot be seen. More obvious symptoms of atrophic gastritis include:

  • Discomfort in the epigastric region (upper, middle region under the ribs).
  • Pain and burning after eating.
  • Feeling of heaviness and nausea. Appear even after a light snack.

These signs characterize the initial form of the disease. If you ignore them and do not go to the doctor for treatment, the symptoms of atrophic gastritis of the stomach will not only intensify, but also be supplemented by such manifestations:

  • Loss of appetite.
  • Heartburn.
  • Increased pain syndrome.
  • Weight loss.
  • Constant weakness.
  • Subfebrile temperature.
  • Increased secretion of hydrochloric acid and its entry into the lumen of the stomach.
  • Increase in the level of general acidity.

Moreover, during this period, a person is especially susceptible to the influence of Helicobacter pylori, a conditionally pathogenic bacterium. For this microorganism, increased acidity is an ideal habitat.

In a small amount, bacteria cannot harm, but in such good conditions they multiply rapidly, which leads to negative consequences. After all, the waste products of bacteria are cytotoxins that increase inflammation of the mucosa.

In addition, against the background of a weakened defense of the body, Helicobacter pylori penetrate deep into, as a result of which the cells of the tissues of the stomach and its glands are poisoned. Because of this, ulcers often occur.

Other alarms

It is important to make a reservation that the above symptoms of atrophic gastritis are not observed in all patients. But here in each of them there are violations associated with the process of absorption of various substances (vitamins, iron, etc.), as a result of which an anemic syndrome begins to develop.

This causes the appearance of symptoms due to a lack of the mentioned elements in the body. They appear as follows:

  • Burning in the mouth.
  • Dyspnea.
  • Drowsiness.
  • fatigue.
  • Apathy.
  • Paleness of mucous membranes and skin.
  • Violation of the sensitivity of the limbs.
  • Pain in the tongue, accompanied by a change in its color.
  • Brittle nails and dry hair.
  • Chest pain.
  • "Air" burp.
  • Instability of the stool (constipation may be replaced by diarrhea).

After an external examination, it is possible to detect plaque. Also, bad breath, a similar taste, as well as hypersalivation (increased salivation) are often observed.

You can not ignore the symptoms of atrophic gastritis of the stomach. This is fraught with serious consequences. Some patients go to the doctor already when their acidity is reduced to alchemy (that is, the acid in the stomach is completely absent).

Consequences

Before proceeding to consider the principles of eliminating symptoms and treating atrophic gastritis with folk and medical means, it is necessary to list the consequences that result from ignoring the disease. These include:

  • Violation of the digestive processes. A neglected state leads to the development of dysbacteriosis.
  • Anemia, beriberi, asthenia.
  • The occurrence of fermentation and putrefaction processes in the stomach.
  • Frequent vomiting, the appearance of blood in saliva.
  • Permanent dehydration.
  • Formation of ulcerative lesions.
  • Decreased secretory function, loss of interest in food, development of exhaustion, which turns into cachexia.
  • Formation in the gastric walls of multiple follicles from lymphoid tissue.
  • Accession of a secondary infection. Possible phlegmonous gastritis.

It is impossible not to mention that with this disease there is a risk of internal gastric bleeding. This complication is a serious threat to life.

Antibiotics

It is very important to choose the right treatment for atrophic gastritis of the stomach, the symptoms and causes of which were listed above. This, of course, is done by the doctor - he prescribes drugs that are suitable for the patient in his particular case, and always those that are gentle on the stomach.

As a rule, the choice is made in favor of such drugs:

  • "Flemoxin Solutab". Penicillin antibiotic of bactericidal action. It can be used from 6 months (but for babies - only in the form of a suspension). The daily dosage for an adult is 1000 - 1500 mg. The specified volume should be divided into morning and evening receptions. As a rule, this antibiotic is combined in combination therapy. It must be taken for at least 10 days.
  • "Panklav". A broad spectrum penicillin antibiotic. It can be taken only from the age of 12, the minimum patient weight is 40 kg. For patients with a moderate degree of health, the norm is 750 mg. The dosage is divided into three doses. If the lesion is severe, you need to take 500 mg 3 times a day. Therapy lasts, as a rule, from 5 to 14 days.
  • Ospamox. It is about the same as the first antibiotic listed. The dosage is similar, 1000-1500 mg / day. In severe cases, it should be increased to 3 g. Ospamox is taken with meals to reduce the negative effects of the drug on the stomach. The duration of therapy is determined individually, but it is at least 7 days.

These drugs are most effective in eliminating symptoms and treating focal atrophic gastritis. And the reviews make sure of that. There are also drugs "Gonoform", "Amosin", "Amoxicar", "Grunamox", "Amoxicillin", "Ecobol" and other antibiotics, but which one will have to be treated will be determined by the gastroenterologist.

proton pump inhibitors

They are also prescribed to eliminate unpleasant symptoms and treat focal atrophic gastritis. Reviews make sure that these drugs help to quickly get rid of mucosal pathologies that have arisen due to disturbed acidity. They reduce the production of hydrochloric acid by blocking the proton pump in parietal cells.

The best means of this group are such antisecretory drugs:

  • "Omeprazole". As a rule, the daily dose is 20 mg. In severe cases and during exacerbation, it is doubled. It is best to take the remedy at night. Be sure to take the tablets with plenty of water. Therapy lasts from 14 to 30 days.
  • Bioprazol. One capsule per day is enough, which contains just 20 mg of active ingredient. It should be noted that this drug is very quickly absorbed in the stomach.
  • "Omezol". A mildly acting drug that is prescribed even for duodenal ulcers. One tablet contains 40 mg of the active ingredient, so the doctor will individually prescribe the dosage. As a rule, one piece per day is enough.
  • "Controller". An inhibitor whose main active ingredient is pantoprazole. It especially lies in the gentle effect on the gastric mucosa. Therefore, the course of treatment is usually long. This is necessary to prevent relapse.
  • "Nolpaza". The drug is similar in action to Controllock. But it is forbidden to take it to people under 18 years of age. The analogue is a medication called "Ultera". Any of the drugs is taken in the morning, the dosage is determined by the doctor.

In addition to these funds, there are also tablets based on rabeprazole and esomeprazole. They are also prescribed to relieve symptoms and treat atrophic gastritis in adults. Preparations with esomeprazole are special in that their components remain in the human body for a long time (this is the reason for the minimum dosages). And rabeprazole drugs are usually indicated for ulcers.

Other drugs

In addition to the above, there are many other medicines that help eliminate the symptoms and treat atrophic gastritis.