a) Blockers of H 2 -histamine receptors : cimetidine, ranitidine, famotidine, nizatidine, roxatidine.

The mechanism of their action is associated with competitive inhibition of the action of histamine on the H 2 receptors of parietal cell membranes and a subsequent decrease in the secretion of hydrochloric acid and pepsin, a decrease in the volume of gastric secretion, while basal, nocturnal and induced secretion of hydrochloric acid is inhibited.

b) Proton pump blockers : omeprazole (omez, losek), lansoprazole, rabeprazole, esomeprazole.

These drugs inhibit the flow of H + ions into the stomach cavity, does not affect the formation of pepsin. Especially effective for gastric and duodenal ulcers resistant to H2-histamine blockers. The mechanism of action is associated with inhibition of the activity of H + K + - ATPase in the parietal cells of the stomach and blockade of the final stage of hydrochloric acid secretion. As a result, basal and inducible secretion is reduced for 24 hours or more, regardless of the nature of the stimulus.

v) Selective M 1 anticholinergics - pirenzepine (gastrozepine), telenzepine.

They block M 1 -cholinergic receptors located on the neurons of the intramural ganglia, which leads to a decrease in the secretion of hydrochloric acid. Improve microcirculation in the mucous membrane of the stomach and duodenum 12.

G) Gastrin receptor blockers: proglumid (milid).

The drug blocks gastrin receptors on the basement membrane, reduces the secretion of hydrochloric acid, increases the resistance of the mucous membrane of the stomach and duodenum 12

3. Antihelicobacter agents: de-nol, amoxicillin, clarithromycin, metronidazole, tetracycline.

H. pylori is found in the stomach in more than 90% of patients with duodenal ulcers, and somewhat less often in gastric ulcers. This microorganism is able to cause an inflammatory process in the wall of the stomach, thereby facilitating the impact of aggressive contents on its mucous membrane. Eradication N.R. in 90% of patients leads to the cure of peptic ulcer. Metronidazole as an anti-Helicobacter agent in Belarus is not recommended due to the high level of resistance of the microorganism.

Schemes of eradication therapy for H. pylori infection (Maastricht Agreement-3, 2005)

First line therapy (triple therapy):

Second line therapy (quadrotherapy):

In 3rd line therapy, a proton pump inhibitor is used 2 times a day, clarithromycin is replaced by levofloxacin

The course of therapy is at least 14 days; 7-day schemes can be applied if high-quality local studies have demonstrated its effectiveness and cost-effectiveness.

Means that activate the system of protection factors:

1. Gastroprotectors- sucralfate (venter), bismuth tripotassium dicitrate (de-nol), misoprostol.

Sucralfate (venter)- a combination of sucrose sulfate and organic ammonium salt. It has a local protective, film-forming effect. In the acidic environment of the stomach, it is selectively fixed in the crater of the ulcer, binding to the proteins of the necrotic tissue.

Misoprostol- a synthetic analogue of prostaglandin E 1, heals ulcers, has a protective effect during long-term treatment with non-steroidal anti-inflammatory drugs.

De-nol(bismuth tripotassium subcitrate) - colloidal bismuth subcitrate, has a bactericidal (against Helicobacter pylori) and cytoprotective action. The colloidal state of the drug contributes to the local formation of a protective insoluble film at the site of ulceration. In addition, de-nol stimulates the formation of prostaglandin E 2 and the secretion of bicarbonates.

Carbenoxolone Na (biogastron) is a herbal preparation from licorice. It enhances the secretion of mucus, increases its viscosity, inhibits enzymes involved in the inactivation of prostaglandins.

2. Reparants- liquiriton, solcoseryl, gastrofarm, sea buckthorn oil, anabolic steroids, vitamin A, U preparations.

Liquiriton- contains the amount of flavonoids from the roots and rhizomes of licorice. Improves ulcer healing.

Solcoseryl- activates capillary blood circulation, oxygen uptake and metabolic processes in pathologically altered tissues, accelerates granulation and epithelialization of the ulcer.

Gastrofarm- the effect of the drug is ensured by the presence of Lactobacillus bulgaris and biologically active products of their vital activity (lactic and malic acid, nucleic acids, a number of alpha-amino acids, polypeptides and polysaccharides), as well as a high content of proteins (25-30%), which have a gastroprotective effect. Stimulates regeneration processes in the mucous membrane of the gastrointestinal tract, normalizes the function of the stomach and intestines, regulates the balance of intestinal microflora.

Sea buckthorn oil- stimulates the regeneration of epithelial cells of the mucous membrane, providing an enveloping and anti-inflammatory effect

Anabolic steroid- stimulate protein synthesis in the body and reparative processes.

Preparations of vitamins A, U- stimulate the regeneration process.

The high content of hydrochloric acid in the stomach is an unfavorable factor and often provokes the development of gastric diseases, the most common: stomach and duodenal ulcers, including stress ulcers of the gastrointestinal tract, gastritis, heartburn, ulcerative colitis. Antisecretory drugs, a list of drugs is often necessary for preliminary review before buying them, in order to better navigate the choice of suitable drugs: by price, form of release, dosage and other features. This group of drugs contributes to a faster healing process (scarring) of the damaged lining of the stomach.

Modern drugs are able to significantly lower the level of acidity for a long time on average from 8 to 24 hours, which is an indisputable advantage of such drugs, since their action allows you to avoid nighttime pain attacks, during the hours when there is a long time break between the last meal - dinner and upcoming breakfast. They are also used in courses to prevent and reduce the risk of relapse.

It should be noted that antisecretory drugs for the treatment of heartburn are used only in cases of its severe forms, when antacid group drugs, such as Almagel, Phosphalugel, Maalox, are not effective. Antacids are able to quickly reduce the level of acid and the therapeutic effect occurs quickly, but their action is short-lived and this is their main drawback.

Before treatment, it is imperative to undergo a gastroscopy in order to exclude other diseases, including malignant ones, which can be masked as diseases of the housing and communal services.

Note: Drugs are often produced in the form of capsules. Some people have difficulty swallowing them. In this case, it is recommended to open the capsule and pour its contents into a tablespoon of applesauce and immediately swallow it with water. Such advice is contained in the instructions for the Omez capsules.

The best antisecretory drugs - list, release form, price

In all of these drugs, the main active substance is "omeprazole".

1. "Omez".

• Capsule release form: 10 mg-30 pcs., 20 mg-30 pcs., 40 mg-28 pcs. and powder for injection - 40 milligrams.
• Take half an hour before meals twice a day for 20 mg.
• Made in India Dr. Reddy's.
• The cost of 30 capsules of twenty milligrams is 175 rubles.

2. "Omez insta".

• Available in the form of a powder of 5 sachets in a package of twenty milligrams.
• The powder should be diluted in one or two tablespoons of water and taken half an hour before meals. Depending on the disease, according to the instructions, the powder is consumed from one to two times a day.
• Manufacturer: Dr. Reddy`s, India.
• The cost of 1 package (5 packages) is 76 rubles.

3. "Omeprazole".

Sales leader. Quality affordable medicine.

• Available in capsules of 20 mg by different manufacturers of 10, 20 and 40 milligrams.
• The first capsule should be taken in the morning as desired: before, after or during meals, once or twice a day, as directed.
• The price of a package of 20 capsules of twenty milligrams of Russian manufacturers: Sintez AKOMP 32 rubles, Ozone 45 rubles, Canonpharma 50 rubles, Hemofarm 70 rubles.
• The drug is also produced by foreign manufacturers in Switzerland, the Czech Republic, Israel, its cost is much more expensive.

4. Losek Maps.

• Available in tablets. Pack of 14 or 28 pcs. 20 mg.
• The first tablet is taken in the morning. Daily intake from one to two pieces, depending on the disease according to the instructions.
• An effective drug as part of complex therapy for the treatment of peptic ulcer caused by Helicobacter pylori. Reduces daily acidity up to 80%.
• Manufacturer: AstraZeneca.
• The only drawback of the drug is its cost of 585 rubles. per pack 28 pcs. 20 milligrams.

5. "Ultrop".

• Available in capsules of 10, 20 milligrams in the amount of 14 and 28 pieces per pack.
• The advantage of the drug is the ability to treat gastrointestinal ulcers caused by the bacterium Helicobacter pylori as part of combination therapy.
• The capsule is washed down with water before the first meal. According to the instructions, depending on the form of the disease, the daily norm is one or two pieces.
• Production: KRKA, Slovenia.
• The cost of packing 28 pcs. twenty milligrams is 309 rubles, which is significantly lower than the cost of a similar drug "Losek Maps" (also kills the bacterium Helicobacter pylori).

6. "Gastrozol".

• Release form in capsules. Packed in 14 or 28 pieces of 20 mg per pack.
• The medicine can be taken once a day for 20 or 40 mg at the same time as meals, as well as before or after meals.
• It should be noted that of the contraindications for taking medicinal capsules, the instructions only list hypersensitivity, which is quite rare in the group of antisecretory drugs.
• Manufacturer: Pharmstandard, Russia.
• The cost of 28 pieces of 20 mg is 144 rubles.

7. "Ortanol"

• It is produced in capsules of 10, 20, 40 mg in an amount of 7, 14 or 28 pcs.
• A feature of the drug is a short course of treatment up to 14 days (on average it is 3 weeks). The initial daily dose is 20 mg, and with a decrease in painful symptoms, it decreases by 10 mg per day and can be increased if they increase.
• The medicine is not recommended for heartburn, if it bothers no more than twice a week.
• Manufacturer: Sandoz, Switzerland.

It should be noted that it is more profitable to buy capsules in 10 mg packaging, because according to the treatment regimen, a variable intake of first 20 mg, and then 10 mg of the drug is required.

• The cost of packing 28 pcs. 10 mg - 176 rubles.

8. "Omitoks".

• Produced in capsules in the amount of 30 pcs. 20 mg.

This antiulcer drug is by far the best drug for the treatment of gastrointestinal ulcers caused by Helicobacter pylori, when judged by cost criteria.

• Depending on the type of disease, the drug is taken once or twice a day for 20-40 mg. Treatment of an ulcer provoked by the bacterium Helicobacter pylori is performed for 7 days as part of antiviral therapy.
• The medicine can be taken both before and after meals.
• Manufacturer: Shreya, India.
• The cost is 131 rubles.

All of the above drugs have a number of contraindications. Read the instructions carefully.

Acute pancreatitis is an acute aseptic inflammation of the pancreatic tissue of a demarcation type, which is based on acute dystrophy, enzymatic autoaggression with necrobiosis of pancreatocytes and subsequent outcome in necrosis of the gland tissue and surrounding structures with the addition of an endogenous secondary purulent infection or in sclerosis of the pancreas with atrophy of its glandular apparatus .

In the modern clinic of urgent surgery, acute pancreatitis ranks third in the number of urgently hospitalized patients, second only to acute appendicitis and acute cholecystitis. Despite the constant improvement of treatment tactics and the introduction of new diagnostic and therapeutic technologies, over the past decade, mortality in acute pancreatitis has ranged from 7-15%, and in destructive forms of pancreatitis reaches 40-80%.

To date, a huge number of works devoted to the problem of acute pancreatitis have been published. However, until now, most of the provisions regarding the etiology, pathogenesis, classification and treatment tactics for this pathology remain highly debatable. It is generally accepted that acute pancreatitis is a polyetiological disease. At the same time, American authors consider it to be the main cause of alcohol abuse, German - cholelithiasis, Chinese and Vietnamese authors - ascariasis. Nevertheless, two groups of etiological factors of this disease are traditionally distinguished. The first group includes factors that determine the violation of the outflow of pancreatic secretions from the acini through the intralobular ducts to the main pancreatic duct and further to the duodenum, which leads to a sharp increase in pressure in the ductal system of the pancreas (hypertensive-ductal factors). Intraductal hypertension occurs with spasm, inflammatory, cicatricial and neoplastic stenosis of the major duodenal papilla, including the sphincter of Oddi, choledocholithiasis. Spasm of the sphincter of Oddi may be the result of both various neuro-reflex influences from the receptors of the hepatogastroduodenal zone, and direct irritation of the sympathetic and parasympathetic parts of the nervous system. Excitation of the vagus nerve causes hypersecretion of pancreatic juice, spasm of the sphincter of Oddi, the occurrence of stasis and hypertension in the pancreatic duct system. It has been established that long-term alcohol intake in relatively large doses directly causes an increase in pressure in the small ducts of the pancreas. The etiological factors belonging to the second group lead to the primary lesion of acinar cells under conditions of normal intraductal pressure (primary acinar factors). It is known that the primary lesion of pancreatic acinar cells can occur with local disorders of hemoperfusion, allergic reactions, metabolic disorders, hormonal imbalance, toxic effects, infections, and trauma to the pancreas. The role of the alimentary etiological factor of acute pancreatitis can be reduced to the following. Foods rich in proteins and fats, alcohol cause a pronounced secretion of pancreatic juice, rich in protein and poor in bicarbonates, which, with inadequate outflow, can cause the development of alimentary pancreatitis. damage to the acinar apparatus and the development of metabolic pancreatitis . It has been noted that excessive consumption of protein-rich foods can lead to sensitization of the body with protein metabolites, which leads to the development of allergic pancreatitis. Thus, the main etiological factors of acute pancreatitis can be called the following: cholelithiasis, pathology of the terminal common bile duct and OBD, alcohol abuse , injuries (including operating ones) of the pancreas, vascular diseases, metabolic disorders, infections, intoxications, autoallergic conditions. It has been experimentally shown and clinically confirmed that the most severe forms of acute pancreatitis develop with a combination of three etiological factors:

pancreatic hypersecretion;

acute intraductal hypertension;

intratubular activation of pancreatic enzymes.

The pathogenesis of acute pancreatitis is currently also the subject of heated debate. It is believed that the development of acute pancreatitis leads to a violation of the intracellular formation and transport of pancreatic enzymes, as well as intraacinar activation of proenzymes by hydrolases. The trigger mechanism of pathological reactions, which are the basis of the inflammatory-necrotic lesion of the pancreas, is the release of activated pancreatic enzymes from acinar cells, which are normally present in the form of inactive proenzymes. At the same time, it is generally accepted today that the processes of autolysis are primarily due to the action of lipolytic enzymes. The activation of lipases occurs when the proenzymes of the latter come into contact with bile acids and enterokinases. This situation occurs during hydraulic destruction of acini due to intraductal hypertension, which is mainly a consequence of hypersecretion of the pancreas and biliary-pancreatic or duodeno-pancreatic reflux with stenosis or insufficiency of the sphincter of Oddi and duodenal hypertension. It is assumed that alcohol has not only a direct toxic effect on pancreatocytes, but also causes the formation of protein microconglomerates that occlude small pancreatic ducts. Note that pancreatic lipase does not damage a healthy cell. The damage is caused by the action of phospholipase A, leading to the destruction of cell membranes, which makes it possible for lipase to enter the cell. When this mechanism is implemented, loci of fatty pancreonecrobiosis with a perifocal demarcation ridge are formed. If the pathobiochemical process is limited to this, then fatty pancreatic necrosis is formed. In the event that, with excessive accumulation of fatty acids in the gland tissue, the pH reaches 3, 4-4, 3, intracellular trypsinogen is transformed into trypsin. At the same time, trypsin activates proenzymes of lysosomes, as well as other proteinases that cause proteolysis of pancreatocytes. Activated elastase lyses the walls of blood vessels, interlobular connective tissue bridges, which contributes to the rapid spread of enzymatic autolysis in the pancreas and in the surrounding structures. Under the action of trypsin, all pancreatic proenzymes (elastase, carboxypeptidase, chymotrypsin proenzyme), proenzymes of the kallikrein-kinin system, fibrinolytic enzymes and hemocoagulation profactors are activated, which ultimately leads to local and general pathobiochemical disorders with a possible ending in the form of multiple organ failure syndrome. . It is customary to single out the pre-infectious stage of the disease, in which aseptic inflammatory and necrotic foci are formed, and the phase of infectious complications - infected pancreatic necrosis, infected pancreatic necrosis with pancreatogenic abscess, retroperitoneal phlegmon.

Thus, one of the fundamental moments of the complex of pathological reactions, united by the concept of "acute pancreatitis", is intraductal hypertension in the pancreas. Wherein the main component of the increase in intraductal pressure is the secretion (in some situations - hypersecretion) of pancreatic juice.

The traditional classification of acute pancreatitis, adopted by practical surgeons, is a clinical and morphological classification that distinguishes acute edematous pancreatitis and destructive forms of pancreatitis - fatty pancreatic necrosis, hemorrhagic pancreatic necrosis, and also provides for the possible development of early and late complications. S. F. Bagnenko, A. D. Tolstoy, A. A. Kurygin (2004) distinguish the following clinical forms of acute pancreatitis, corresponding to the pathophysiological phase of its course:

I phase-enzymatic, is the first five days of the disease. During this period, the formation of pancreatic necrosis of various lengths, the development of endotoxemia (the average duration of hyperenzymemia is 5 days), and in some patients - multiple organ failure and endotoxin shock. The maximum period for the formation of pancreatic necrosis is three days, after this period it does not progress further. However, in severe pancreatitis, the period of formation of pancreatic necrosis is much shorter (24-36 hours). It is advisable to distinguish two clinical forms: severe and non-severe acute pancreatitis.

• Severe acute pancreatitis. The frequency of occurrence is 5%, lethality is 50-60%. The morphological substrate of severe acute pancreatitis is widespread pancreatic necrosis (large-focal and total-subtotal), which corresponds to severe endotoxicosis.
• Mild acute pancreatitis. The incidence rate is 95%, lethality is 2-3%. Pancreatic necrosis in this form of acute pancreatitis either does not form (pancreatic edema), or is limited and does not spread widely (focal pancreatic necrosis - up to 1.0 cm). Mild acute pancreatitis is accompanied by endotoxicosis, the severity of which does not reach a severe degree.

II phase-reactive(2nd week of the disease), characterized by the reaction of the body to the formed foci of necrosis (both in the pancreas and in the parapancreatic tissue). The clinical form of this phase is a peripancreatic infiltrate.

III phase-meltdown and sequestration(starts from the 3rd week of the disease, can last several months). Sequesters in the pancreas and retroperitoneal tissue begin to form from the 14th day from the onset of the disease. There are two possibilities for this phase:

• aseptic melting and sequestration - sterile pancreatic necrosis; characterized by the formation of postnecrotic cysts and fistulas;
• septic fusion and sequestration - infected pancreatic necrosis and necrosis of parapancreatic tissue with the further development of purulent complications. The clinical form of this phase of the disease is purulent-necrotic parapancreatitis and its own complications (purulent-necrotic swells, abscesses of the retroperitoneal space and abdominal cavity, purulent omentobursitis, purulent peritonitis, arrosive and gastrointestinal bleeding, digestive fistulas, sepsis, etc.) .

It should be noted that not all authors share the point of view on the evolution of pathomorphological changes in acute pancreatitis and suggest the possibility of a primary destructive process (hemorrhagic pancreatic necrosis) without previous acute edematous pancreatitis and fatty pancreatic necrosis. Perhaps this is due to the fact that, due to the well-known social background, patients are hospitalized already at the stage of hemorrhagic pancreatic necrosis or in the presence of purulent complications. However, the majority of researchers support the idea of ​​the continuity of the morphological phases of acute pancreatitis. So, M. Schein (2004) calls pancreatitis "a disease of four weeks." And this is quite understandable, both from the point of view of pathomorphology, and from the pragmatic point of view of a practicing American surgeon. Indeed, the first two weeks - persistent complex conservative treatment, in the subsequent period - surgical interventions from minimally invasive (laparoscopy, transparietal punctures) to very aggressive ones (necrsequestrectomy, omentopancreatobursostomy, opening of pancreatogenic abscesses and phlegmon of the retroperitoneal space). Since, within the framework of this section, the author did not aim to continue the discussion about therapeutic tactics in acute pancreatitis (primarily about the indications, timing and volume of surgical benefits), the main attention is paid to the issue of conservative treatment of patients with this pathology. It should be noted that, according to a number of authors (A. D. Tolstoy, 2003, M. Schein, 2004), it is the pathogenetically substantiated complex conservative therapy for acute pancreatitis that is of decisive importance for the outcome of the disease. This is especially true in acute edematous pancreatitis, as it prevents the transition of this form of pancreatitis to pancreatic necrosis. No less relevant is intensive conservative therapy for already formed foci of fatty or hemorrhagic destruction, which in this case prevents the spread of inflammatory-necrotic foci to previously intact tissue. In addition, given the primary asepsis of the process in acute pancreatitis in the initial period of the disease, from the standpoint of common sense, it is advisable to actively therapeutic treatment aimed at stopping pathological processes in the pancreas itself, preventing and treating the syndrome of pancreatogenic toxemia, and preventing purulent-septic complications.

Currently, the fundamental provisions of the conservative treatment of acute pancreatitis are set out in all guidelines for emergency abdominal surgery. Let us remind the reader of them with some comments. So, in acute pancreatitis are shown:

1. Measures aimed at inhibiting the exocrine function of the pancreas: A) "Cold, hunger and rest" (local hypothermia, strict diet, bed rest); B) Drug suppression of pancreatic secretion: cytostatics (5-fluorouracil, tegafur), inhibitors of gastric secretion (antisecretory drugs - H2-blockers, PPIs), opioid receptor agonists (dalargin), pancreatic ribonuclease, somatostatin and its synthetic analogues (octreotide).
2. Antispasmodic therapy: myotropic antispasmodics (drotaverine, papaverine), anticholinergics (platifillin, atropine), infusions of glucose-novocaine mixture.
3. Measures aimed at inactivation of pancreatic enzymes circulating in the blood and inhibition of the cascade of reactions of the kallikrein-kinin system: protease inhibitors - aprotinin, ε-aminocaproic acid.
4. Relief of pain syndrome: non-steroidal anti-inflammatory drugs, opioid (of course, with the exception of morphine) analgesics, regional novocaine blockades.
5. Correction of hypovolemic and water-electrolyte disorders, improvement of microcirculation, inhibition of free radical oxidation: infusions of crystalloids, colloids (hydroxystarch preparations, gelatins), perfluoroorganic emulsions, albumin, fresh frozen plasma, specific and nonspecific antioxidants.
6. Detoxification therapy and methods of afferent detoxification: dextran infusions, forced diuresis, extracorporeal detoxification (hemo-, lympho- and enterosorption, plasmapheresis, ultrahemofiltration).
7. Replenishment of energy costs (at least 3500 kcal / day): parenteral nutrition, balanced enteral tube nutrition.
8. Correction of enteral insufficiency syndrome: prevention or relief of intestinal paresis, decompression of the small and large intestines, enteral lavage, the use of enterosorbents, antihypoxants.
9. Preventive prescription of antibacterial drugs: III generation cephalosporins, fluoroquinolones, metronidazole, with developed pancreatic necrosis - carbapenems (meropenem).
10. Posyndromic therapy.

In the works of various authors over the past five to ten years, the evolution of treatment tactics in patients with acute pancreatitis from aggressive surgical to conservative expectant is clearly traced. The modern approach to the treatment of patients with acute pancreatitis dictates the need to select a specific variant of the ongoing therapy, taking into account the staging of the course of pancreatitis, taking into account the dynamics of laboratory parameters and data from instrumental studies - ultrasound, computed tomography, magnetic resonance imaging.

It should be noted that an indispensable condition for the treatment of patients with any clinical and morphological form of acute pancreatitis is the observance of the main condition - the creation of rest for the pancreas. This is achieved by suppressing the production of enzymes by pancreatocytes, as a result of which the release of enzymes that lyse proteins (trypsin, chymotrypsin, elastase) and phospholipid cell membranes (phospholipases, cholesterol esterase) is significantly reduced. Thus, the resting state of the pancreatocyte contributes to the regression of autolysis and prevents necrotic tissue changes. In this regard, in the complex therapy of acute pancreatitis, the leading place is occupied by drugs that directly or indirectly inhibit the exocrine function of the pancreas. The maximum therapeutic effect is achieved with synergistic suppression of enzyme synthesis at the level of the pancreas, excretion and inactivation of enzymes already circulating in the blood.

Historically, the first class of compounds used for this purpose in acute pancreatitis were cytostatics - 5-fluorouracil, tegafur. The disadvantage of these drugs is the inhibition of leukopoiesis, impaired immunogenesis, the occurrence of hypo- and dysproteinemia. The use of these drugs is justified in verified pancreatic necrosis in order to maximally suppress the secretory function of the pancreas and thereby reduce the level of pancreatic enzymes in plasma. Previously, drugs of the protease inhibitor class were widely used to inhibit pancreatic secretion, but it is now established that protease inhibitor drugs are active only in the blood. As a rule, protease inhibitors do not enter the pancreatic tissue in sufficient concentrations and cannot effectively perform their function in relation to pancreatic juice enzymes. In addition, protease inhibitors have an autoimmunizing effect. To suppress the exocrine function of the pancreas, the use of opioid receptor agonists (dalargin), which selectively accumulate in pancreatocytes and inhibit the synthesis of pancreatic proenzymes, is justified. Pancreatic ribonuclease has a similar mechanism of action, which destroys the matrix RNA of cells, due to which protein synthesis by pancreatocytes is inhibited. The drugs of choice for acute pancreatitis include a synthetic analogue of the somatostatin hormone - octreotide, which has a pronounced inhibitory effect on the exocrine function of the pancreas due to the activation of specific D-receptors of pancreatocytes. The main directions of its action are inhibition of basal and stimulated secretion of the pancreas, stomach, small intestine, regulation of the activity of the immune system, production of cytokines, cytoprotective effect. In addition, octreotide acts in the same way on the parietal and chief cells of the stomach, helping to reduce acid formation. The usual dosing regimen for octreotide is 300–600 mcg/day. with three intravenous or subcutaneous injections.

A pathogenetically substantiated method of inhibiting pancreatic secretion is the use of drugs that reduce gastric secretion - antisecretory drugs. To understand the mechanism of action of antisecretory drugs in acute pancreatitis, one should briefly dwell on the regulation of pancreatic secretion. The regulation of pancreatic juice secretion is carried out by neurohumoral mechanisms, with the main importance being given to humoral factors - gastrointestinal hormones (secretin, cholecystokinin-pancreozymin), which are activated with the participation of releasing peptides secreted in the duodenal mucosa. Secretin enhances the production of the liquid part of the juice, and cholecystokinin-pancreozymin stimulates the enzymatic activity of the pancreas. Insulin, gastrin, bombensin, bile salts, serotonin also enhance the secretory activity of the gland. The secretion of pancreatic juice is inhibited by: glucagon, calcitonin, somatostatin. The process of pancreatic secretion includes three phases. Cephalic (complex reflex) phase due mainly to reflex excitation of the vagus nerve. Gastric phase associated with the effects of the vagus nerve and gastrin secreted by the antral glands when food enters the stomach. During intestinal (intestinal) phase When acidic chyme begins to enter the small intestine, the rate of pancreatic secretion becomes maximum, which is primarily associated with the release of secretin and cholecystokinin by the cells of the intestinal mucosa. Thus, there is a direct relationship between the secretion of hydrochloric acid by the parietal cells of the stomach, a decrease in intraduodenal pH, the production of secretin in the duodenal mucosa and an increase in the secretion of pancreatic juice. That is why to inhibit the secretion of pancreatic juice, reduce intraductal pressure in the pancreas and, ultimately, to reduce intrapancreatic enzyme activation, measures are used to suppress the secretion of hydrochloric acid in the stomach - a physiological stimulator of pancreatic secretion. A decrease in the acidity of gastric juice causes a less pronounced acidification of the duodenum, as a result of which the release of secretin, the main hormone that stimulates the excretory function of the pancreas, decreases.

It should be noted that, despite the widespread (and in a number of clinics - obligate) use of antisecretory drugs for the treatment of patients with acute pancreatitis, systematic studies on this issue have not been conducted either in Russia or abroad. From individual messages it is known that:

The use of omeprazole in the complex treatment of patients with acute pancreatitis and exacerbation of chronic pancreatitis contributes to more rapid relief of abdominal pain, normalization of the clinical picture, relevant instrumental and laboratory parameters (Zvyagintseva T. D. et al., 2003; Minushkin O. N. et al. , 2004) ;

The clinical efficacy of omeprazole in acute pancreatitis is the highest among antiulcer drugs. Omeprazole has a high lipophilicity, easily penetrates into the parietal cells of the gastric mucosa, where it accumulates and activates at an acidic pH. Rabeprazole has a shorter duration of action than omeprazole. In acute pancreatitis, the daily dose of omeprazole was 40 mg (M. Buchler et al., 2000);

Today, based on the principles of evidence-based medicine, it can be confidently stated that the effectiveness of PPIs in acute pancreatitis is significantly higher compared to H2-histamine receptor blockers (K. Bardhan et al., 2001, data from a meta-analysis by N. Chiba et al. , 1999).

Given the fact that in order to exclude acidification of the duodenum, intragastric pH should not be lower than 4, the optimal regimen for the use of the parenteral form of omeprazole (Losek) in acute pancreatitis should be considered a bolus injection of 80 mg of the drug followed by continuous infusion at a rate of 4 mg / h.

The need for the use of antisecretory drugs in acute pancreatitis is due to two more circumstances. Very often (at least in 20% of cases) acute pancreatitis is combined with peptic ulcer. At the same time, the presence of at least one causal relationship is obvious: ulcer formation - acute pancreatitis. Firstly, it is possible to develop an inflammatory-necrotic process in the pancreas due to the penetration of ulcers into the head and body of the gland. Secondly, peptic ulcer, as a rule, is combined with severe duodenal motility disorders, which, being realized through duodenal hypertension, leads to the formation of duodenal-pancreatic reflux. In these complex clinical situations, the control of gastric acid formation is one of the main goals of treatment. Therefore, in this case, the use of antisecretory drugs, including long-term, has absolute indications. Finally, another indication for the appointment of antisecretory drugs in acute pancreatitis is the prevention of stress erosive and ulcerative damage, the need for which is especially relevant in severe acute pancreatitis with the development of large-focal pancreatic necrosis, purulent-septic complications and multiple organ failure syndrome.

In conclusion, we want to emphasize once again that the use of a complex of modern intensive care measures (antisecretory therapy, other inhibitors of pancreatic secretion and proteolytic enzymes, detoxification agents) in patients with acute pancreatitis, taking into account the staging and individual dynamics of the disease, as well as timely prevention of purulent complications pancreatic necrosis will undoubtedly improve the results of treatment of patients with acute pancreatitis, reduce the stay of patients in the hospital, reduce the need for invasive treatments and, most importantly, reduce mortality.

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COURSE WORK ON THE TOPIC:

"The value of antisecretory drugs in the treatment of chronic gastritis and peptic ulcer"

Performed

student:

Borisovova L.A.

Head Kulchenkova A.A.

Moscow 2016

INTRODUCTION

1.1 Etiology and pathogenesis

1.2 Classification of chronic gastritis and peptic ulcer disease

1.3 Diagnosis and treatment

2.1 Nature and chemical classification of antisecretory drugs

2.2 Mechanism of action of antisecretory drugs

Practical part of the study

CONCLUSION

BIBLIOGRAPHY

APPS

gastritis chronic drug antisecretory

INTRODUCTION

Chronic gastritis and peptic ulcer of the stomach and duodenum in many countries are one of the most urgent problems of gastroenterology. This is due to their high prevalence of the disease in young and middle age, a high rate of recurrence and complications with improper treatment. The results of recent research and observation of patients after the introduction of fundamentally new types of therapy have completely changed the existing ideas not only about the causes and mechanisms of these diseases, but also about the possibilities of treating them therapeutically.

According to modern data, diseases of the stomach and duodenum account for 58-65% in the structure of gastroenterological pathology. Chronic gastritis and peptic ulcer are not rare diseases and occur in 3.4% of urban residents and 1.9% of rural residents. Over the past 10 years, the incidence of chronic gastritis has increased by 27%, of peptic ulcer - by 2.5 times, the number of frequently recurrent and complicated forms has increased. This can be associated with incorrect, outdated approaches to the diagnosis and treatment of gastroduodenal pathology. Establishing the role of Helicobacter pylori infection in the development of this group of diseases has significantly changed approaches to both therapy and their prevention. Untimely diagnosis and inadequate treatment of these diseases contribute to a significant decrease in the health indicators of children, and then adults.

The purpose of the work is to study the correct mechanisms for diagnosing chronic gastritis, gastric and duodenal ulcers, conducting staged therapy and preventing these diseases using antisecretory drugs, based on modern ideas about the etiology and pathogenesis.

The object of the study is antisecretory drugs used to treat chronic gastritis and peptic ulcer.

The subject of the study is the use of antisecretory drugs in the treatment of chronic gastritis and peptic ulcer.

This study will explore and suggest that the use of antisecretory drugs should occupy one of the main places in the treatment of chronic gastritis and peptic ulcer disease.

To achieve the goal of the work, a number of tasks were set:

3) describe the mechanism of action of antisecretory drugs;

Theoretical part of the study

CHAPTER 1. MEDICAL ASPECTS OF CHRONIC GASTRITIS AND ULCER

In modern gastroenterology there is no more controversial problem than the treatment of patients with peptic ulcer and chronic gastritis. Despite the huge number of publications, today there is also no single approach to the etiology, pathogenesis, method of treatment, and prevention.

1.1 Etiology and pathogenesis

Chronic gastritis is a disease with a chronic relapsing course, which is based on inflammatory and dystrophic lesions of the gastric mucosa, which are accompanied by a violation of its secretory, motor and endocrine function.

Its prevalence: among all diseases - 35% of cases; among diseases of the stomach - 85%. Chronic gastritis affects 40-50% of the adult population of the world. The prevalence of the disease depends on the place and living conditions of people and is clearly correlated with Helicobacter pylori infection.

Peptic ulcer is a chronic disease of the stomach or duodenum with a relapsing course, prone to progression, which is based on the formation of a peptic ulcer in the mucous membrane of the stomach or duodenum during an exacerbation followed by scarring.

There are a number of exogenous and endogenous factors, including genetic ones, leading to the emergence and development of gastroduodenal ulcers. For some factors, the association with peptic ulcer is proven, for others it remains controversial so far.

At one time it was believed that the influence of spicy, spicy and rough food leads to an increase in the secretory function of the stomach. Studies have not shown an overwhelming prevalence of peptic ulcer in those countries where spicy and spicy food is commonplace. It is not worth ignoring the nutritional factor completely. After all, any patient who has suffered from peptic ulcer disease can say with certainty which products he cannot tolerate because of the development of discomfort in him.

Convincing evidence in favor of the effects of alcohol, smoking and coffee abuse is also not currently available. Proved that

smoking causes ischemia and has a direct cytotoxic effect on the gastric mucosa. Smoking and frequent coffee consumption contribute to the occurrence of relapse, so the rejection of bad habits is considered a prerequisite for the treatment of peptic ulcer.

Currently, negative mental emotions should be considered as one of the non-specific harmful factors that provoke exacerbation of not only peptic ulcer, but also many other diseases. It is worth remembering that gastric secretion directly depends on the functional state of the nervous system, and therefore sedatives are also widely used in the treatment of peptic ulcers.

It has been proven that certain groups of drugs cause acute erosive and ulcerative lesions of the gastric mucosa by reducing gastrocytoprotection (decrease in the number of prostaglandins in the cells of the mucous membrane, increased reverse diffusion of hydrogen ions) and contribute to the exacerbation of an existing peptic ulcer.

Drugs that damage the stomach lining include:

NSAIDs (aspirin, indomethacin, etc.),

corticosteroids,

antibacterial agents,

Digoxin, theophylline, reserpine,

Preparations of iron, potassium.

Along with exogenous factors, there are also endogenous favorable factors for the development of the disease. It is believed that their significance in the development of peptic ulcer is much higher.

Endogenous factors:

genetic predisposition;

Hyperproduction of hydrochloric acid and pepsin;

Gastroduodenal motility disorders;

Age and gender.

In patients with duodenal ulcer hereditary burden reaches 30-40%.

Genetically distinguish the following traits:

An increase in the number of parietal cells,

Excessive secretion of gastrin in response to food stimulation,

Increased serum pepsinogen

Gastroduodenal motility disorders

Deficiency of pepsin inhibitors in the mucosa.

Duodenal ulcers occur 1.5 times more often and develop more severely in persons:

With blood group 0 (1), Rh +,

The presence in the blood of some HLA antigens (U-5, B-15, B-35).

At a young age, duodenal localization of ulcers is absolutely more common, and in older age groups, differences in incidence are reduced due to an increase in the proportion of gastric ulcers.

In healthy people, there is an inverse relationship between the secretion of hydrochloric acid and the motor-evacuation function of the stomach:

The higher the secretion of hydrochloric acid, the lower its motor activity, and vice versa.

To date, in the world literature, hyperproduction of hydrochloric acid and Helicobacter pylori infection are considered as examples. More than 95% of patients with duodenal ulcers and 90% of patients with gastric ulcers have Helicobacter pylori infection.

1.2 Classification of chronic gastritis and peptic ulcer

The classification of chronic gastritis was adopted in 1990 at the IX International Congress of Gastroenterologists. In clinical practice, three types of chronic gastritis are most common:

1. Surface

With a predominant lesion of the antrum of the stomach, which is most often associated with Helicobacter pylori (type B gastritis), in which normal or even increased secretion of hydrochloric acid persists for a long time.

Chronic gastritis type B is manifested by symptoms that are characteristic of peptic ulcer:

Hungry and night pains in the epigastrium,

Nausea

belching sour,

heartburn.

Characterized by a tendency to constipation.

All symptoms are due to an increase in acidity in response to damage to the antrum of the stomach. The disease may be asymptomatic.

2. Autoimmune

Fundic gastritis (type A gastritis), in the formation of which autoimmune mechanisms take part. It is characterized by the detection of antibodies to parietal cells and intrinsic factor, as well as a high level of gastrin in the blood serum.

Chronic type A gastritis is initially asymptomatic until B12-deficiency megaloblastic anemia develops.

Sometimes the clinic is characterized by symptoms of gastric dyspepsia:

- (dull pain and heaviness in the epigastrium after eating, belching, nausea, unpleasant taste in the mouth)

Signs of intestinal dyspepsia (flatulence, diarrhea).

Type A gastritis is often combined with other autoimmune diseases:

Hashimoto's thyroiditis,

Addison's disease

3. Chemical

Reflux gastritis (gastritis type C), which is characterized by a focal lesion of the fundus of the stomach due to a cytotoxic effect on the mucous membrane of the contents of the duodenum 12 during duodenogastric reflux. Often develops in the stump of the operated stomach with small bowel reflux. Close to this type of gastritis, caused by drug-induced damage to the gastric mucosa.

Chronic gastritis type C is manifested by the following symptoms:

Pain and feeling of heaviness in the epigastrium during sleep or immediately after eating,

Nausea,

Often has an asymptomatic course.

Other infectious gastritis (not Helicobacter pylori-associated) are caused by:

Viruses

microbes

Morphological changes in chronic gastritis include symptoms such as:

Inflammation,

Atrophy,

Cell renewal disorders, including metaplasia and dysplasia.

The classification of peptic ulcer disease (ICD-10) was adopted by WHO in 1992. According to her, the following types of peptic ulcer are distinguished:

K.25 Gastric ulcer including erosions (acute) of the stomach

K.26 Duodenal ulcer including erosions (acute)

K.28 Gastrojejunal ulcer.

To date, the classification of gastric ulcers proposed by H. Johnson (1965) is widely used in practice, according to which three types of gastric ulcers are distinguished:

Type I - ulcers of the lesser curvature of the stomach.

Type II - stomach ulcers with duodenal ulcers.

Type III - prepyloric ulcers (in the area up to 3 cm above the pylorus).

Type II and III ulcers in most cases belong to hypersecretory and, according to clinical characteristics, are close to duodenal.

In 1990, A. Johnson, based on this classification, slightly expanded it and proposed to additionally distinguish two more types of ulcers:

IV type - acute superficial ulcers.

Type V - gastric ulcers that develop as a result of Zollinger-Ellison syndrome (in combination with a duodenal ulcer or without it).

There is no single generally accepted clinical classification of peptic ulcer disease. Basically, it is now customary to distinguish between two clinical forms - duodenal ulcers and stomach ulcers, which is of great importance in establishing indications for surgery and choosing a method of therapeutic treatment. Thus, peptic ulcer is classified:

By localization

stomach ulcer:

2. Duodenal ulcer:

3. Combination of gastric ulcer and duodenal ulcer.

According to the clinical form:

1. Acute ulcer.

2. Chronic ulcer.

By process phase

1. Aggravation.

2. Incomplete remission.

3. Remission.

By clinical course:

1. Peptic ulcer with a latent course.

2. Mild (rarely recurs) disease.

3. Moderate (1-2 relapses per year).

4. Severe (3 relapses per year or more) or continuously relapsing disease, development of complications.

According to the morphological picture:

1. Small ulcer (less than 0.5 cm in diameter).

2. An ulcer of medium size (0.5-1.0 cm).

3. Large ulcer (1.0-3.0 cm).

4. Giant ulcer (more than 3.0 cm).

According to the presence of complications:

1. Complicated by bleeding.

2. Complicated by perforation: open (into the free abdominal cavity), covered.

3. An ulcer that penetrates or is callous.

4. Ulcer, complicated by cicatricial deformities of the stomach and duodenum.

5. Malignant ulcer.

In turn, the complications of peptic ulcer can be divided into the following groups:

1) ulcerative-destructive - penetration, perforation, bleeding

2) inflammatory - periduodenitis;

3) ulcerative cicatricial - stenosis, deformity;

4) complications associated with malignancy of the ulcer.

By etiology:

1. Hp-positive ulcer;

2. Hp-negative ulcer;

3. Medication;

4. Stressful;

5. With endocrine diseases (Zollinger-Ellison syndrome, hyperparathyroidism);

6. With a disease of the internal organs.

1.3 Diagnosis and treatment

The methods of instrumental diagnosis of gastritis and ulcers are functional diagnostics:

Determination of gastric secretion by fractional sounding or intragastric pH-metry;

Endoscopy;

Morphological study;

X-ray examination of the gastrointestinal tract;

Diagnosis of H. pylori infection (bacteriological examination - sowing of a biopsy specimen of the mucous membrane on a differential diagnostic medium);

Morphological: histological - staining of bacteria in a histological preparation of the mucous membrane according to:

Cytological - staining of bacteria in smears-imprints of the gastric mucosa according to Giemsa,

Determination of waste products of helicobacteria:

Urease - determination of urease activity in a biopsy of gastric mucosa in a liquid or gel-like medium containing a substrate, a buffer and an indicator; -

Respiratory - determination of 14C or 13C isotopes in the exhaled air, released as a result of the splitting of labeled urea in the patient's stomach under the action of urease of the bacterium H. pylori;

ELISA - determination of antibodies to H. pylori;

PCR - determination of H. pylori using polymerase chain reaction in feces.

Treatment of gastritis and ulcers consists of a regimen, diet and pharmacotherapy. Adherence to the regime should be manifested in the normalization of lifestyle: the elimination of stress, if necessary, the use of sedatives.

The diet should follow the principles:

The purpose of the diet is mechanical, chemical, thermal sparing of the mucous membrane of the gastrointestinal tract, normalization of secretion and gastric motility.

The diet is complete in terms of energy value and chemical composition. Diet - 5-6 times a day. All food should be steamed, boiled and rubbed through mechanisms or a hair sieve.

Basic principles of therapeutic nutrition for gastritis and peptic ulcer disease:

1. Creation of the greatest rest of the mucous membrane of the stomach and duodenum.

2. Exclusion of products with a strong juice effect.

3. All food is given pureed.

4. The inadmissibility of the introduction of large volumes of food at one time.

5. Frequent and fractional meals.

6. Exclusion of too cold and too hot food (not

below 15°C and not higher than 65°C).

7. Restriction of table salt to 10-12 g per day.

8. High nutritional value of the diet (proteins, fats, carbohydrates, mineral salts, vitamins A, B, C). The chemical composition of the diet: 100 g of proteins, 100-110 g of fats, of which vegetable oil, 400-450 g of carbohydrates. Caloric content of the diet is 3000-3200 kcal.

The most valuable product for this category of patients is milk, but some patients do not tolerate it well. In these cases, it should be drunk in small doses, always in a warm form, it can be diluted with weak tea or coffee.

Diet example table number 1

As part of diet number 1, you can cook a huge variety of delicious and healthy soups. Soups based on vegetable broth with the addition of vermicelli, rice, and various vegetables are welcome. You can fill such soups with cream or add an egg to the broth.

Instead of the usual rich bread, you can use dried bread or crackers, which can be added directly to the soup.

As for meat dishes, lean chicken or rabbit are recommended as part of a healthy diet - the most dietary types of meat. Baked veal or turkey. A few days a week, you can cook lean fish for a couple or in the form of fish cakes with a creamy sauce.

A variety of dairy products such as milk and cream, fresh sour cream and kefir, non-acidic cottage cheese and curdled milk help maintain the health of the digestive tract. If you are tired of dairy products, you can always treat yourself to cheesecakes that do not lose the beneficial properties of the dairy product. Milk can be added to egg dishes - you get a tender, tasty omelet. It is also better to cook porridge with milk - they will be both healthy and satisfying.

Restrictions

In order not to overwork the stomach, you should give up rye bread and puff pastry, fatty meat and various horrors that actively leave the diet of people who care about health: canned food, salty cheeses, hot sauces and marinades. White cabbage, mushrooms, sorrel, spinach, onions, cucumbers, carbonated drinks, black coffee are also contraindicated.

Sample menu for the day

1st breakfast: soft-boiled egg, rice milk porridge, tea with milk. 2nd breakfast: baked apple with sugar. Lunch: vegetable soup, steamed meatballs with mashed potatoes, fruit mousse. with milk sauce, vegetable stew, tea with milk. At night: milk and an apple or banana.

Pharmacotherapy - depends on the type of gastritis and ulcers. For example, chronic gastritis type B - it is advisable to treat by eradication of H. pylori

The scheme of eradication therapy is presented in table. one.

HCG type A - has no special treatment. With concomitant exocrine pancreatic insufficiency (steatorrhea) - pancreatic enzymes. In the presence of megaloblastic anemia - intramuscular injection of B12 1000 mcg for 6 days, then for a month 1 time per week, then continue throughout life 1 time in 2 months

CG type C - normalization of the motility of the digestive tract and binding of bile acids. Effective prokinetics (motilium) (6-10 g per day) in combination with antacids (maalox).

MOTILIUM (Belgium):

Dosage form

Tablets, suspension

Pharmacotherapeutic group

Antiemetic drugs

Indications for use Motilium:

* dyspepsia

* nausea and vomiting

* nausea and vomiting of an infectious, organic or functional nature

* gastroesophageal reflux

Contraindications:

* perforation of the gastrointestinal tract or obstruction of mechanical etiology

* hypersensitivity to domperidone or other components of Motilium;

* reception against the background of ketoconazole in oral forms of release.

Method of application and dosage Motilium

Children and adults take 10 mg 15-30 minutes before meals 3 times a day. If necessary, you can take the drug before bedtime. The maximum dose is 80 mg / day. For children over 12 years of age and adults, the dosage can be doubled as needed.

Motilium suspension is used at the rate of 2.5 ml / 10 kg of the child's body weight (which is a dose of 250 μg per 1 kg of body weight). The dosage can be doubled if necessary only for children older than 1 year. The maximum dose is 2.4 mg per 1 kg of body weight per day, but not higher than 80 mg / day.

MAALOX (France).

Dosage form

suspension

Pharmacotherapeutic group

Aluminum-based astringents, coatings and antacids

Pharmacological properties:

Antacid

enveloping, -

adsorbent

Indications for use Maalox:

Peptic ulcer of the stomach and duodenum in the acute phase

Acute or chronic gastritis)

Reflux esophagitis,

diaphragmatic hernia,

Duodenitis,.

Contraindications:

hypersensitivity,

Severe renal dysfunction

Alzheimer's disease,

Usage Precautions:

Long-term use (more than 20 days) requires medical supervision

Side effects:

Nausea,

Pain in the epigastric region

Modern schemes for the treatment of peptic ulcer:

One-week triple therapy with proton pump inhibitors at standard dose twice a day, one of the drugs (omeprazole 20 mg, pantoprazole 40 mg, rabeprazole 30 mg, esomeprazole 20 mg) plus clarithromycin (500 mg 2 times a day) or amoxicillin (1000 mg 2 times a day) and tinidazole (500 mg 2 times a day).

2. One-week triple therapy with bismuth preparations: denol (120 mg 4 times a day) + clarithromycin (500 mg 2 times a day) + tinidazole (500 mg 2 times a day).

3. One-week quadruple therapy, which makes it possible to achieve the eradication of H. pylori strains resistant to the action of known antibacterial substances: a proton pump inhibitor in a standard dose + denol (120 mg 4 times a day) + clarithromycin (500 mg 2 times a day) + tinidazole ( 500 mg 2 times a day) or metronidazole (250 mg 4 times a day)

OMEPROZOL(Russia)

Belonging to ATX-classification:

Drugs affecting the digestive tract and metabolism

Dosage form

Pharmacotherapeutic group

For the treatment of peptic ulcer of the stomach and duodenum - Blockers of H2-histamine receptors

Indications for use Omeprazole:

peptic ulcer

Reflux esophagitis

Zollinger-Ellison syndrome.

Contraindications:

Pregnancy, breastfeeding.

Method of application and dosage Omeprazole

With exacerbation of peptic ulcer and reflux esophagitis, the drug is prescribed at a dose of 0.02 g once in the morning (before breakfast). Capsules should be swallowed whole with a small amount of liquid.

Side effects:

Rarely - dizziness,

In some cases, depression

RABEPROZOL(Russia)

Release form of the drug

tablets, coated, soluble in the intestine 10 mg; blister 10 cardboard pack 1;

Indications for use:

Peptic ulcer of the stomach and duodenum in the acute phase;

peptic ulcer of the stomach and duodenum associated with Helicobacter pylori (in combination with antibiotics);

Gastroesophageal reflux.

Contraindications for use:

Pregnancy, lactation (breastfeeding),

Hypersensitivity to rabeprazole sodium or substituted benzimidazoles

Side effects:

Rarely - dry mouth,

Dosage and administration:

Taken inside. Single dose - 10-20 mg. The frequency and duration of use depend on the indications and treatment regimen.

EZOMEPROZOL (Russia).

Composition, form of release of the drug "Esomeprazole"

The drug is available in the form of tablets with a dosage of 20 and 40 mg of the active ingredient esomeprazole, as well as in the form of a powder intended for the preparation of a solution for injection (40 mg vial). The tablets are coated, the dissolution of which occurs in the intestine.

Indications:

Gastroesophageal reflux disease

Erosive reflux esophagitis (treatment),

Prevention of relapses in patients with cured esophagitis, symptomatic treatment of GERD.

As part of combination therapy: eradication of Helicobacter pylori, duodenal ulcer associated with Helicobacter pylori, prevention of recurrence of peptic ulcers in patients with peptic ulcer associated with Helicobacter pylori

Contraindications:

lactation period,

Hypersensitivity to esomepromazole.

Dosage:

Taken inside. The dose is 20-40 mg 1 time / day. The duration of admission depends on the indications, treatment regimen, effectiveness.

In severe liver failure, the maximum dose is 20 mg / day.

Side effects:

Often: headache,

Rare: dermatitis,

Dizziness,

Dry mouth.

CLARITHROMICIN (Russia)

Dosage form

capsules 250mg

Pharmacotherapeutic group

Antibiotics - macrolides and azalides

Indications for use Clarithromycin

Upper respiratory and ENT infections,

Exacerbation of chronic bronchitis,

bacterial and atypical pneumonia), skin and soft tissues,

Peptic ulcer of the duodenum and stomach caused by Helicobacter pylori (combination therapy).

Contraindications

hypersensitivity,

severe liver disease,

porfiria,

Pregnancy and lactation.

Side effects

Nausea,

cholestatic jaundice,

Hives,

Stevens-Johnson syndrome, etc.)

Anaphylactoid reactions.

TINIDAZOL (Russia)

Belonging to ATX-classification:

Ingredients of Tinidazole

The active substance is tinidazole.

Dosage form

coated tablets 500mg

Pharmacotherapeutic group

Indications for use Tinidazole

Acute and chronic trichomoniasis,

Amoebiasis and Giardiasis

cutaneous leishmaniasis,

Anaerobic and mixed infections of various localization (abscess of the lungs, brain, infective endocarditis).

Contraindications

increased sensitivity,

blood diseases,

Diseases of the central nervous system in the active phase,

Pregnancy (I trimester), breastfeeding,

Children's age up to 12 years

Side effects

Dyspeptic disorders

Dizziness

Allergic reactions.

DE NOL (France)

in a blister 8 pcs.; in a box of 7 or 14 blisters.

Characteristic

Bismuth drug.

pharmachologic effect

Pharmacological action - gastroprotective, antiulcer, antibacterial.

Indications

Peptic ulcer of the stomach and duodenum in the acute phase (including those associated with Helicobacter pylori);

Chronic gastritis and gastroduodenitis in the acute phase (including those associated with Helicobacter pylori);

Irritable bowel syndrome, occurring mainly with symptoms of diarrhea;

Functional dyspepsia, not associated with organic diseases of the gastrointestinal tract.

Contraindications

Decompensated renal failure;

Pregnancy;

lactation period;

Children's age up to 4 years;

Hypersensitivity to the drug.

METRONIDAZOL (Russia)

Belonging to ATX-classification:

Ingredients of the drug Metronidazole Nycomed

The active substance is metronidazole.

Dosage form

tablets 250mg, tablets 500mg, suppositories 1g, solution for infusion 5mg/ml

Pharmacotherapeutic group

Means for the treatment of trichomoniasis, amebiasis and other protozoal infections

Indications for use Metronidazole Nycomed

amoebiasis,

Anaerobic infections of bones and joints, skin and soft tissues,

female genital

lower respiratory tract

pseudomembranous colitis,

Helicobacter pylori eradication,

Dosage

For the eradication of Helicobacter pylori - 500 mg 3 times a day. within 7 days (as part of combination therapy, for example, a combination with amoxicillin 2.25 g / day).

Contraindications

Hypersensitivity

Pregnancy, lactation,

Children's age (excluding cases of amoebiasis).

Side effects

Headache

Neutropenia (leukopenia),

Nausea,

erythematous rashes,

skin itch,

Dark discoloration of urine

CHAPTER 2. STUDYING THE USE OF ANTISECRETORY DRUGS IN THE TREATMENT OF CHRONIC GASTRITIS AND ULCER

With the development of the pharmaceutical industry for the treatment of:

Erosive-destructive diseases of the gastroduodenal zone,

Gastroesophageal reflux disease (GERD)

With the development of reflux esophagitis,

Pathology associated with Hp infection,

in adults, a wide range of drugs of the proton pump inhibitor group is offered as initial therapy and the "gold standard"

2.1 Essence and chemical classification of antisecretory drugs

Antisecretory agents inhibit the secretion of hydrochloric acid and pepsin. The synthesis of hydrochloric acid is controlled by three types of receptors:

H-2-histamine,

Gastrinov

Thus, 4 groups of antisecretory drugs are distinguished:

M-cholinolytics,

Proton pump inhibitors

Blockers of gastrin receptors.

2.2 Mechanism of action of antisecretory drugs

H2-blockers in the treatment of chronic gastritis and peptic ulcer have been used since the mid-70s and are currently one of the most common antiulcer drugs.

The main antisecretory effect of H2-blockers is manifested as a result of blocking H2-histamine receptors in the gastric mucosa. Due to this, the production of hydrochloric acid is suppressed and an antiulcer effect is carried out. The drugs of new generations differ from the first drug of the cimetidine group in the degree of suppression of the nocturnal and total daily secretion of hydrochloric acid, as well as the duration of the antisecretory effect. (see table No. 2 in the appendix)

Drugs vary in bioavailability values:

Cimetidine has a value of -60-80%,

Ranitidine - 50-60%,

Famotidine - 30-50%,

Nizatidine - 70%,

Roxatidine - 90-100%.

Removal of drugs is carried out by the kidneys, and 50-90% of the dose taken is unchanged. The duration of the half-life is different for the drugs of the group: cimetidine, ranitidine and nizatidine for 2 hours, famotidine - 3.5 hours, roxatidine - 6 hours.

CIMETIDIN (Russia)

Dosage form

tablets 200mg

Pharmacotherapeutic group

H2-histamine receptor blockers and similar drugs

Indications for use:

peptic ulcer of the stomach and duodenum,

Hyperacidity of gastric juice (reflux esophagitis, gastritis, duodenitis),

Zollinger-Ellison syndrome,

pancreatitis,

Gastrointestinal bleeding.

Contraindications

Liver and / or kidney failure,

Pregnancy, breastfeeding

Children and adolescence (up to 14 years).

Side effects

Deterioration of the excretory function of the liver,

Decreased absorption of vitamin B12,

Neutro- and thrombocytopenia,

Allergic reactions (skin rashes).

In the treatment of chronic gastritis, 4 drugs of the group are most often used.

RANITIDIN (India)

Release form

10 tab. in aluminum strips. 1, 2, 3, 4, 5 or 10 strips in a carton box. (150-300mg)

Blocker of H-2 receptors of the 2nd generation,

Compared with cematidine, it has 5 times greater antisecretory activity,

Lasts longer - up to 12 hours.

Virtually no side effects

Rare: headache,

Nausea,

Tablets of 150 mg are taken 1 time in the morning after meals and 1-2 tablets in the evening before bedtime. Other regimens are possible - 1 tablet 2 times a day or 2 tablets 1 time at night. Treatment must be continued for several months or years, maintenance dose - 1 tablet at night.

Contraindications:

Pregnancy;

Lactation;

Children's age up to 12 years;

Hypersensitivity to ranitidine or other components of the drug.

FAMOTIDIN (Serbia)

Tablets of 20 mg and 40 mg, ampoules of 20 mg.

3rd generation H2 receptor blocker,

The antisecretory effect exceeds ranitidine by 30 times.

In complicated peptic ulcers, 20 mg in the morning and 20-40 mg in the evening before bedtime are prescribed. It is possible to take only 40 mg at bedtime for 4-6 weeks, maintenance therapy - 20 mg once at night for 6 weeks.

Side effects

Dry mouth

Headache

allergic reactions

sweating

Contraindications:

Pregnancy;

lactation period;

Children's age up to 3 years with a body weight of less than 20 kg (for this dosage form);

Hypersensitivity to famotidine and other histamine H2 receptor blockers.

NIZITIDIN (Russia)

Release form. Capsules of 0.15 and 0.3 g in packs of 30 pieces; concentrate for infusion in vials of 4, 6 and 12 ml (1 ml contains 0.025 g of nizatidine).

4th generation blocker.

Assign tablets of 150 mg 2 times a day or 2 tablets at night for a long time.

Gastroduodenal ulcers heal within 4-6 weeks in 90% of patients.

Side effect.

Possible nausea,

Rarely - damage to liver tissue;

Drowsiness,

sweating,

Contraindications. Hypersensitivity to the drug.

ROXATIDINE (India)

Release form:

Roxatidine Precautions

Before starting treatment, it is necessary to exclude the presence of malignant tumors in the gastrointestinal tract.

H2-blocker of the 5th generation.

Tablets of 150 mg are prescribed 1 time per day or 2 tablets 1 time at night.

Contraindications:

hypersensitivity,

Impaired liver and kidney function,

Pregnancy, breastfeeding (should be discontinued for the period of treatment),

Childhood.

Side effects:

Headache

visual impairment

gynecomastia,

Impotence, transient decrease in libido,

Skin rash, itching.

Proton pump inhibitors (PPI) play a major role in the treatment of chronic gastritis and peptic ulcer disease.

(fig. No. 1 see in the appendix)

The high therapeutic efficacy of proton pump inhibitors is explained by their pronounced antisecretory activity, which is 2-10 times higher than that of H2-blockers. Taking an average therapeutic dose once a day (regardless of the time of day) suppresses the level of gastric acid secretion during the day by 80-98%, and for H2-blockers, the same indicator is 55-70%.

Ingestion of PPIs promotes entry into the acidic environment of the stomach, sometimes causing premature conversion to sulphenamides, which are poorly absorbed in the gut. Therefore, they are used in capsules that are resistant to the action of gastric juice.

The half-life of omeprazole is 60 minutes, pantoprazole is eliminated in 80-90 minutes, and lansoprazole is 90-120 minutes. Diseases of the liver and kidneys do not significantly affect these indicators.

Omeprazole, Pantoprazole (see above in diagnosis and treatment).

LANSOPROZOL (Russia)

Release form

Lansoprazole 30mg caps N30

pharmachologic effect

Anti-ulcer agent.

Take orally 30 mg 1 time per day (morning or evening). With anti-Helicobacter therapy, the dose is increased to 60 mg per day.

Side effects:

Allergic reaction

Headache

photosensitivity

Contraindications:

hypersensitivity,

Malignant neoplasms of the gastrointestinal tract,

Pregnancy (especially the first trimester)

M-cholinolytics are the oldest means. the first of them for the treatment of peptic ulcers used preparations of belladonna and atropine. For a long time, atropine was considered as the main medicine for chronic gastritis and peptic ulcers. However, the pharmacodynamics of drugs is manifested in an indiscriminate effect on numerous M-cholinergic receptors in the body, which leads to the development of many serious side effects. Among the group of M-anticholinergic drugs, the selective M1-anticholinergic pirenzepine is the most effective, blocking M1-cholinergic receptors at the level of intramural ganglia and inhibiting. the influence of the vagus nerve on the secretion of hydrochloric acid and pepsin, without having an inhibitory effect on the M-cholinergic receptors of the salivary glands, heart and other organs.

Pirenzepine is the only one included in group A02B (ATX code A02BX03), however, in terms of clinical efficacy, it is inferior to both proton pump inhibitors and H2 blockers. Therefore, its use in modern therapy is limited.

PIRENZEPIN (Germany)

Forms of release and composition:

Pirenzepine tablets of 0.025 and 0.05 g - in a package of 50 pcs.

Powder Pirenzepine 0.01 g in an ampoule - in a package of 5 ampoules with a solvent.

Pharmacological group

M-anticholinergic.

(after 2-3 days) switch to oral administration.

Substance use:

Peptic ulcer of the stomach and duodenum chronic - hyperacid reflux esophagitis;

Erosive and ulcerative lesions of the gastrointestinal tract, incl. caused by antirheumatic and anti-inflammatory drugs;

Stress ulcers of the gastrointestinal tract;

Zollinger-Ellison syndrome;

Bleeding from erosions and ulcerations in the upper gastrointestinal tract.

Contraindications

Hypersensitivity.

Application restrictions

Glaucoma, prostatic hyperplasia, tachycardia.

Side effects of the substance Pirenzepine

Dry mouth

paresis of accommodation,

Allergic reactions.

Dosage and administration

Inside, in / m, in / in. Inside - 50 mg in the morning and evening 30 minutes before meals with a small amount of water. The course of treatment is at least 4 weeks (4-8 weeks) without interruption.

In severe forms of peptic ulcer of the stomach and duodenum, it is administered intramuscularly and intravenously, 10 mg every 8-12 hours.

In the course of many years of searching for inhibitors of gastrin receptors and creating a number of drugs of this type, there were many difficulties, and their widespread use in practical medical therapy has not yet begun. A non-selective blocker of gastrin receptors is proglumide (code A02BX06). The clinical effect is consistent with the first generation of H2-blockers, but the drug has the advantage of a small number of side effects.

In the Russian Federation, gastrin receptor blockers are not registered.

2.3 Safety and appropriateness of use of the main representatives of antisecretory agents

Histamine receptor blockers in the treatment of chronic gastritis and peptic ulcer have proven to be highly effective. There are a number of side effects of drugs that are characteristic mainly for cimetidine. It is able to provoke an antiandrogenic effect, which is observed as a result of long-term use (often in high doses). The use of cimetidine also causes an increase in the level of prolactin in the blood, the occurrence of galactorrhea and amenorrhea, a decrease in the number of spermatozoa, the progression of gynecomastia and impotence.

H2-blockers of new modifications (ranitidine, famotidine, nizatidine and roxatidine) do not have such effects. They do not exhibit both anti-androgenic properties and are not capable of penetrating through the blood-brain barter, and, accordingly, do not provoke neuropsychiatric disorders.

Abrupt withdrawal of H2-blockers, especially cimetidine, can lead to the development of "rebound syndrome", which is accompanied by secondary hypersecretory reactions.

Thanks to many studies, the higher efficacy of PPIs in the treatment of exacerbations of peptic ulcer disease has been confirmed compared to drugs of the H2-blocker group.

Proton pump inhibitors have a very high safety profile, especially for short (up to 3 months) courses of therapy.

In isolated cases, side effects appear in the form of allergic reactions, skin rashes or bronchospasm. Intravenous administration of omeprazole provoked isolated cases of visual and hearing impairment.

Long-term continuous use of high-dose PPIs (omeprazole 40 mg, pantoprazole 80 mg, lansoprazole 60 mg) causes:

hypergastrinemia,

Progression of the phenomena of atrophic gastritis,

Thus, antisecretory drugs occupy a central place in the treatment of patients with acid-dependent pathologies. To date, the most effective among them are drugs from the group of proton pump inhibitors.

Practical part of the study.

CHAPTER 3

3.1 Organization and methods of research

The study involved 64 patients with endoscopically proven chronic gastritis and peptic ulcer who were treated from January 2014 to September 2015. Exclusion criteria were active peptic ulcer, tumors of the upper alimentary canal, malignant neoplasms of other organs, severe cardiac, renal and hepatic insufficiency, kidney disease, anemia (hemoglobin concentration<10 г / дл), беременность и лактация.

Patients who did not undergo control endoscopy were withdrawn from the experiment during the study. After obtaining informed consent to participate in the study, patients were prescribed one of four PPIs (omeprazole, lansoprazole, pantoprazole, or esomeprazole in a sealed package) for 8 weeks.

All PPIs were prescribed once a day (in the morning): omeprazole 20 mg, pantoprazole 40 mg, lansoprazole 30 mg and esomeprazole 40 mg. The sample consisted of 34 men and 30 women aged 36 to 85 years. The mean age was (53.2 ± 9.5) years.

Endoscopy was performed by the same physician using a high resolution endoscope to examine the upper GI tract before treatment and at 8 weeks after PPI administration.

All patients were instructed to keep a diary in which they could report on a 6-point symptom intensity scale (heartburn and acid reflux) before treatment and during 7 days of therapy. Mild symptoms were considered those that did not affect the activity of patients. Moderate symptoms were considered to be those that affect daily activities but do not significantly alter the patient's work performance. Severe symptoms interfere with normal daily activities of patients. Patients noted the intensity of symptoms each morning compared to the previous day.

Daily changes in major symptoms were analyzed separately. The ultimate goal of the study was to find out how different antisecretory drugs improve symptoms during the first week of treatment.

Statistical analysis of intergroup data was carried out using a standard Microsoft Office Excel software package using the F-test.

3.2 Description of study results

As a result of the studies, there were no severe side effects of PPI use. None of the patients took additional antacids to relieve symptoms while on PPIs.

On fig. 2 shows daily changes in the average score of the main symptoms of gastritis and peptic ulcer - in all patients who took PPIs.

Rice. 2. Daily changes in the symptoms of CG and PU under the influence of antisecretory drugs

Although there was no significant difference between the groups in the intensity of pain symptoms before PPI prescription, in those who took esomeprazole, it decreased already on the 1st and 2nd day of taking the drug compared with those who were treated with omeprazole, lansoprazole and pantoprazole, respectively. The difference between esomeprazole and other PPIs disappeared after the 5th day of administration.

Although symptoms improved faster with esomeprazole than with omeprazole, pantoprazole, and lansoprazole, all studied drugs were effective during the 1st week of treatment, which was endoscopically confirmed.

Thus, the study found that esomeprazole at a dose of 40 mg/day is more effective than omeprazole (20 mg/day), pantoprazole (40 mg/day) and lansoprazole (30 mg/day) in the rate of relief of major symptoms of chronic gastritis and peptic ulcer, although after several days of treatment, this effect and the percentage of healing of erosions (at the 8th week of treatment) did not differ significantly regardless of the type of PPI.

CONCLUSION

Based on the results of the course work, the goal of this work, set in the introduction, was achieved:

Based on modern ideas about the etiology and pathogenesis, to study the correct mechanisms for diagnosing chronic gastritis, gastric and duodenal ulcers, conducting staged therapy and preventing these diseases with the help of antisecretory drugs.

To achieve this goal, the following tasks were implemented:

1) describe the etiology, pathogenesis and main methods of treatment of chronic gastritis and peptic ulcer;

2) define antisecretory drugs, carry out their chemical classification;

3) describe the features of the pharmacodynamics of antisecretory drugs;

4) to determine the legitimacy and safety of using the main representatives of the studied pharmacological group in the treatment of gastroduodenal pathology;

5) to study the features of the treatment of chronic gastritis and peptic ulcer with the use of antisecretory drugs.

After analyzing all the data I studied in the process of writing a term paper, we can draw the following conclusions:

Chronic gastritis is a disease with a chronic relapsing course, which is based on inflammatory and dystrophic lesions of the gastric mucosa, accompanied by a violation of its secretory and motor function. Peptic ulcer is a chronic disease of the stomach or duodenum with a relapsing course, prone to progression, which is based on the formation of a peptic ulcer in the mucous membrane of the stomach or duodenum during an exacerbation followed by scarring.

Antisecretory agents are drugs that inhibit the secretion of hydrochloric acid and pepsin. The synthesis of hydrochloric acid is controlled by three types of receptors:

H-2-histamine,

Gastrinov

M-cholinergic receptors.

Depending on the pharmacodynamic characteristics, 4 groups of antisecretory drugs are distinguished:

H-2-histamine receptor blockers,

M-cholinolytics,

Proton pump inhibitors

Blockers of gastrin receptors.

The safest and most clinically effective drugs are proton pump inhibitors.

An empirical study found that esomeprazole 40 mg/day was more effective than omeprazole (20 mg/day), pantoprazole (40 mg/day) and lansoprazole (30 mg/day) in relieving major symptoms of chronic gastritis and peptic ulcer disease, although after several days of treatment, this effect and the percentage of healing of erosions (at the 8th week of treatment) did not differ significantly regardless of the type of PPI.

BIBLIOGRAPHY

Isakov V.A. Safety of proton pump inhibitors during long-term use. Klin. pharmacol. and therapy. - 2004.

Lapina T. L. Proton pump inhibitors: several questions on theory and practice // Farmateka. 2006. Journal

Treatment and prevention of disorders of the mucous membrane of the gastrointestinal tract in therapeutic practice / Vertkin A. L., Vovk E. I., Naumov A. A. // Klin, prospect. gastroenterol., hepatol. -- 2009.

Pasechnikov V.D. Keys to the choice of the optimal proton pump inhibitor for the treatment of acid-dependent diseases // Ros. magazine gastroenterol., hepatol. and coloproctol. - 2004.

Rapoport S.I., Lakshin A.A., Rakitin B.V., Trifonov M.M. pHmetry of the esophagus and stomach in diseases of the upper digestive tract / Ed. acad. RAMS F.I. Komarova.-- M.: ID Medpraktika6M, 2005.

Samsonov A.A. Proton pump inhibitors are drugs of choice in the treatment of acid-dependent diseases // Pharmateka.-- 2007.

APPS

Table 1 H. pylori eradication therapy

First line
1st component	2nd component	3rd component
PPI: omeprazole (OMEZ) 20 mg 2 times a day	Clarithromycin (Lecoclar) 500 mg 2 times a day	Amoxicillin (Ospamox) 1000 mg twice daily or metronidazole 500 mg twice daily
Second line
1st component	2nd component	3rd component	4th component
PPI: omeprazole (OMEZ) 20 mg 2 times a day	bismuth / subcitrate 120 mg 4 times a day	Metronidazole 500 mg 3 times a day	Tetracycline 500 mg 4 times a day

Table 2. Comparative pharmacodynamics of H2-blockers

A drug	Night secretion, %	Total secretion, %	Duration of action, hour
Cimetidine
Ranitidine
famotidine
Nizatidine
Roxatidine

Rice. 1. Pharmacodynamics of proton pump inhibitors

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Heartburn is the reflux of gastric juice into the esophagus. This symptom is often the result of an unhealthy lifestyle (alcohol consumption, obesity, smoking) or indicates a disease of the digestive organs (peptic ulcer, gastritis with high acidity), especially with the simultaneous occurrence of pain in the stomach.

A huge number of medicines for heartburn in pharmacies, advertising assurances about the rapid elimination of an unpleasant symptom can inspire confusion. When choosing them, you should know the features of taking certain drugs, existing contraindications and focus on the optimal ratio of effectiveness and cost.

Antacids

Heartburn medications that neutralize acidity are similar in action to soda. However, unlike the latter, they do not stimulate a further increase in acid production and irritation of the mucous membrane due to the release of carbon dioxide. The group of antacids are agents based on magnesium and aluminum.

Important! Antacids are indicated for short-term heartburn, relief comes after a few minutes. Reception of most funds is limited to 5 days.

List of acid-reducing medications:

• Magnesium and aluminum hydroxide - Gastracid (inexpensive), Almagel, Maalox (disposable sachets for taking), Gastal. Acidity when they are taken decreases quite smoothly, the risk of constipation / diarrhea is minimal, but the effect lasts only up to 2 hours. These funds are completely contraindicated up to 6 years old, older children are prescribed only by a doctor and in compliance with the exact dosage and duration of treatment.
• Phosphalugel. Sachets for one dose (can be diluted with water). Aluminum phosphate often provokes constipation, therefore, during the use of this drug, you should increase the amount of fluid you drink.
• Rennie. Rennie chewable tablets are the best antacid to quickly eliminate heartburn even in pregnant women (confirmed safety at recommended doses). This drug is preferred when the specific taste of other antacids (Almagel, Maalox) is not accepted. Contraindicated under 12 years of age. Simultaneous administration with antibiotics, cardiac glycosides, iron-containing agents is undesirable (reduces their absorption).
• Vikair, Vikalin. The cheapest remedy used in medical practice since Soviet times. They contain a plant component - calamus rhizomes. Well relieve spasm; along with antacid, have a laxative effect. Contraindicated in children and pregnant women, patients with renal insufficiency. Do not be afraid of dark stool, this effect will disappear after the drug is discontinued.
• Relzer. The liquid agent has an antacid and carminative (combats flatulence) effect. One of the few drugs approved for use by young children and pregnant women. In order to avoid undesirable consequences (vomiting, constipation, renal dysfunction), the age dosage should be strictly observed.
• Iberogast. The herbal preparation regulates the peristalsis of the gastrointestinal tract, reduces acidity and protects the gastric mucosa from ulceration. Contraindicated in children and adolescents under 18 years of age, pregnant and breastfeeding.
• Gaviscon. It is considered the lightest antacid. A distinctive feature is the possibility of use in children from 1 year. Available in syrup, powder, mint/lemon flavored chewable tablets.

Antisecretory drugs

Medicines that reduce the production of hydrochloric acid are prescribed exclusively by a doctor. Treatment of heartburn with antisecretory drugs is advisable for long-term unpleasant symptoms that are not eliminated by dietary changes and antacids.

Important! Antisecretory drugs are more effective than antacids. However, the effect after administration is noticeable only after 1 hour. Contraindicated in children, pregnant women.

• Omeprazole (Omez, Gastrozol, Ultop). They are classified as proton pump blockers. Tablets / capsules are effective for prolonged heartburn.
• Rabeprozole. Analogues - Pariet, Beret, Noflux. These are quite expensive drugs, but more effective than omeprazole preparations.
• Esomeprazole (Emanera - cheaper than Nexium). New generation antisecretory agents are effective in the absence of the effect of the above funds. A significant improvement in the condition is observed already after 5 days of admission, the average course for a stomach ulcer is 1 month.

Antiulcer drugs (Ranitidine, Gistak, Kvamatel)

Long-term use of anti-ulcer drugs for heartburn is often accompanied by side symptoms: dry mouth, headache, abdominal cramps, tachycardia. Smoking and the simultaneous use of antacids (the difference between taking should be more than 2 hours) significantly reduces the effectiveness of these funds.

It is worth remembering that any remedy for heartburn is only symptomatic. Self-administration of these funds is advisable only for short-term heartburn. In this case, the therapeutic result will be only if the following recommendations are followed:

• to give up smoking;
• nutrition correction (exclusion of fatty / spicy, milk, alcohol, coffee);
• control over the intake of NSAIDs (aspirin is especially aggressive against the stomach);
• the correct mode of work-rest (full sleep);
• loose clothing (rejection of belts, tight trousers, corsets).

If heartburn occurs against the background of severe pain in the epigastrium, recurrent vomiting and other serious symptoms, you should immediately contact a medical institution. The lack of improvement within 5 days of regular intake of antacid / antisecretory drugs indicates the development of a pathological condition and requires high-precision diagnosis and subsequent complex treatment.