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Lecture notes, cheat sheets
Hospital therapy. Diseases of the digestive tract. Stomach diseases. Peptic ulcer (lecture notes)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE No. 11. Diseases of the digestive tract. Diseases of the stomach. peptic ulcer Peptic ulcer (peptic ulcer) is a chronic, relapsing disease, clinically manifested by a functional pathology of the gastroduodenal zone, and morphologically - by a violation of the integrity of its mucous and submucosal layers, and therefore the ulcer always heals with the formation of a scar. Etiology. The main etiological factor of peptic ulcer disease is the microbial expansion of HP on the surface of the gastric epithelium. The significance of bacterial aggression in the etiology of the disease has been studied since 1983, when J. Warren and B. Marshall reported the discovery of a large number of S-spiral bacteria on the surface of the epithelium of the antrum of the stomach. Helicobacteria are able to exist in an acidic environment due to the production of the urease enzyme, which converts urea (from the bloodstream) into ammonia and carbon dioxide. The products of enzymatic hydrolysis neutralize hydrochloric acid and create conditions for changing the pH of the environment around each bacterial cell, thus providing favorable conditions for the vital activity of microorganisms. Total HP colonization occurs on the surface of gastric epithelial cells, which is accompanied by damage to the epithelium under the action of phospholipases. The latter provide the formation of toxic lecithins and proteinases from bile, causing the destruction of protective protein complexes and mucus. Against the background of "alkalinization" of epithelial cell membranes with ammonia, the membrane potential of the cells changes, the reverse diffusion of hydrogen ions increases, the death and desquamation of the epithelium of the gastric mucosa. All these changes lead to the penetration of HP into the depth of the gastric mucosa. No less important in the development of peptic ulcers are neuropsychic effects, hereditary predisposition, infectious agents, alimentary errors and the intake of certain medications, and bad habits. For the first time, the neurogenic concept of the onset of the disease was formulated by Bergman, who argued that hereditary-constitutional disorders of the autonomic nervous system lead to spasm of the muscles and blood vessels in the stomach wall, ischemia, and a decrease in the resistance of the mucous membrane to the aggressive effects of gastric juice. This theory was further developed by K. N. Bykov and I. T. Kurtsin (1952). They substantiated the corticovisceral theory of ulcerogenesis, which is based on data on changes in higher nervous activity resulting from chronic neuropsychic traumatization. Supplemented and detailed by the doctrine of the biochemical and hormonal links in the regulation of gastric secretion, motility and trophism, this theory of ulcerogenesis has again won many supporters in recent years. Popular among researchers are hereditary factors: the inertia of the main nervous processes, group-specific properties of blood, immunological and biochemical features, hereditary burden syndrome. In the occurrence of peptic ulcer, essential importance was attached to alimentary violations. However, clinical and experimental studies conducted in the last two decades in most cases did not reveal the damaging effect of food products on the gastroduodenal mucosa. The prevalence of peptic ulcer disease among significant contingents of people with different dietary habits also testifies against the leading importance of nutritional factors. Disturbances in the rhythm and regularity of nutrition, long breaks between meals, untimely eating are essential for the occurrence of peptic ulcers. Researchers have expressed relatively conflicting views about the role of alcohol in ulcerogenesis. Alcohol is known to cause atrophic changes in the gastric mucosa. These observations are in conflict with the general concept of ulceration. However, the frequent use of alcohol is accompanied by violations of the diet, qualitative changes in the composition of food, which ultimately can cause peptic ulcer of the stomach and duodenum. The role of medicinal effects in ulcerogenesis is being actively studied. The results of studies published in the literature and our own data indicate that non-steroidal anti-inflammatory drugs and glucocorticoid hormones have the most pronounced ulcerogenic properties. Pathogenesis. The pathogenesis of peptic ulcer disease is still not fully understood. When considering the processes of ulcerogenesis, it is necessary to highlight a number of postulates: 1) characterized by seasonality of exacerbations of peptic ulcer; 2) there is a predominant localization of peptic ulcers in the antropyloroduodenal zone; 3) the presence of hydrochloric acid and pepsin in gastric juice was noted; 4) a high frequency (up to 70%) of spontaneous healing of gastric and duodenal ulcers is noticeable; 5) there is chronic antral gastritis associated with HP; 6) the anthropyloric part of the stomach and the initial part of the duodenum are the "hypothalamus" of the gastrointestinal tract; 7) there is a hereditary predisposition to the occurrence of peptic ulcers; 8) the occurrence of an ulcer, its recurrence and remission are possible in the presence of all of the above factors. Thus, the unified concept of ulcerogenesis is as follows. In a patient with a hereditary predisposition to peptic ulcer in the presence of chronic bacterial gastritis during the period of autumn or spring dishormonosis, only hyperplasia and hyperfunction of endocrine cells secreting gastrin, histamine, melatonin and serotonin are noted. The main hormones and biogenic amines produced by the anthropyloruduodenal zone are involved both in stimulating gastric secretion and changing trophism and cell proliferation, primarily in this zone. Against the background of active bacterial gastritis and duodenitis, favorable conditions arise for ulcer formation. With the formation of a peptic defect, the functional activity of endocrine cells decreases. This leads to a decrease in acid-peptic aggression, an improvement in tissue trophism in the anthropyloroduodenal zone, and the creation of conditions for the healing of gastric and duodenal ulcers, even against the background of the ongoing microbial expansion of HP. In the acute period of peptic ulcer, hyperplasia of α-endorphin-producing cells, which are universal cytoprotectors, is noted. They act as the main protective mechanisms in peptic ulcers and provide the process of self-limitation of the ulcer and its healing, both directly and by stimulating the immune system. At the same time, antibodies against HP, synthesized in the submucosa of the stomach and duodenum, effectively bind to bacterial cells and neutralize HP toxins and contribute to their death. All of the above contributes to the creation of a balance between the so-called factors of aggression and protection factors and the healing of a peptic defect in the gastroduodenal zone. Classification. Classification (Panfilov Yu. A., Osadchuk M. A., 1991) Localization of the peptic defect: 1) gastric ulcer (subcardial and cardiac sections, pyloric part and pyloric canal, lesser and greater curvature); 2) duodenal ulcer (bulb and postbulbar section); 3) ulcers of the stomach and duodenum. The course of peptic ulcer. 1. Easy. The exacerbation of the ulcer is not more than 1 time in 1-3 years, the healing of the peptic defect ends by the 5-6th week from the start of the therapy, the severity of pain and dyspeptic syndromes is moderate. 2. Moderate. Recurrence at least 2 times a year, ulcer epithelialization - within 7-12 weeks, the severity of pain and dyspeptic syndromes. 3. Heavy. Remission periods do not exceed 3-4 months. In addition to severe pain, there are complications. Phases of the disease: 1) exacerbation of ulcer recurrence or functional disorders of the gastroduodenal system; 2) complete remission (in clinical, radiological, endoscopic and functional aspects); 3) incomplete (with the preservation of functional or structural disorders in the gastroduodenal zone). The condition of the mucous membrane of the stomach and duodenum: 1) chronic gastritis; 2) chronic duodenitis. Functional state of the gastroduodenal system Secretion: normal, increased, reduced. Motility: normal, accelerated, slow; evacuation: normal, accelerated, delayed, duodenostasis. Complications: bleeding, perforation, penetration, perigastritis, periduodenitis, cicatricial deformity of the stomach and duodenum. clinical picture. The clinical picture of peptic ulcer is polymorphic. Symptoms depend on the gender and age of the patient, time of year, location and size of the ulcer, personal and social characteristics of the patient, and his professional qualities. The clinic is determined by a combination of signs: the chronic course of the disease from the moment of its onset, the presence of signs of exacerbation and remission of the disease, healing of the defect in the gastric and duodenal mucosa with the formation of a scar. Peptic ulcer is represented by two clinical and morphological variants: gastric ulcer and duodenal ulcer. Traditionally, pain and dyspeptic syndromes are distinguished. The leading clinical sign is pain in the upper abdomen. By the nature of the pain syndrome, it is almost impossible to distinguish between chronic bacterial gastritis and peptic ulcer. Pain in the epigastric region, on an empty stomach, mainly in spring and autumn, is equally common in both peptic ulcer and chronic bacterial gastritis. Relief of pain syndrome with food and medicinal antacids is achieved both in chronic bacterial gastritis and peptic ulcer. Distinctive for duodenal ulcer is only the presence of pain in the epigastric region at night. Vomiting with peptic ulcer is rare. Nausea is much more common with stomach ulcers and duodenal ulcers. Constipation accompanies chronic duodenal ulcer. Symptoms of peptic ulcer disease are determined by the number of ulcerative defects and their localization. Multiple stomach ulcers are 3 times more common in men. The clinical picture in this case depends on the localization of peptic defects. With ulcers in the body of the stomach, dull pain in the epigastrium without irradiation, which occurs 20-30 minutes after eating, and nausea are noted. With ulcers of the subcardial region, dull pains under the xiphoid process, radiating to the left half of the chest, are characteristic. Combined gastric ulcers and duodenal ulcers are a combination of an active gastric ulcer and a healed duodenal ulcer. They are characterized by long-term preservation of the pain syndrome, persistent course of the disease, frequent relapses of the disease, slow scarring of the ulcer and frequent complications. Extrabulbous ulcers include ulcers located in the region of the bulboduodenal sphincter and distal to it. Their clinical picture has its own characteristics and has much in common with duodenal ulcers. They occur mainly in patients aged 40-60 years. Postbulbar ulcers are severe and prone to frequent exacerbations, accompanied by massive bleeding. Pain localized in the right upper quadrant of the abdomen, radiating to the back or under the right shoulder blade, occurs in 100% of cases. The intensity, severity of pain, which subsides only after taking narcotic analgesics, brings patients to severe neurasthenia. Seasonality of exacerbations in extra-bulbous ulcers is recorded in almost 90% of patients. In many patients, gastrointestinal bleeding becomes a cardinal symptom. Ulcers of the pyloric canal are characterized by a symptom complex called the pyloric syndrome: epigastric pain, nausea, vomiting, and significant weight loss. The exacerbation of the disease is very long. Against the background of intensive antiulcer therapy, the ulcer scars within 3 months. Abundant blood supply to the pyloric canal causes massive gastric bleeding. Diagnostics. In the uncomplicated course of a peptic ulcer, there are no changes in the general blood test; a slight decrease in ESR and slight erythrocytosis are possible. When complications arise in blood tests, anemia appears, leukocytosis - when the peritoneum is involved in the pathological process. There are no changes in the general analysis of urine. In the biochemical analysis of blood in cases of complicated course of peptic ulcer, changes in the parameters of the sialic test, C-reactive protein, DPA reaction are possible. The traditional method of research in the pathology of the stomach is the determination of the acidity of gastric contents. Various indicators are possible: elevated and normal, in some cases even reduced. A duodenal ulcer occurs with high acidity of gastric juice. In X-ray examination, a peptic ulcer is a "niche" - a depot of barium suspension. In addition to such a direct radiographic symptom, indirect signs of a peptic defect are important in the diagnosis: hypersecretion of the contents of the stomach on an empty stomach, evacuation disorders, duodenal reflux, cardia dysfunction, local spasms, convergence of mucosal folds, cicatricial deformity of the stomach and duodenum. Gastroduodenoscopy with biopsy is the most reliable method for diagnosing peptic ulcer. It allows you to assess the nature of changes in the mucous membrane in the edge of the ulcer, in the periulcerous zone and guarantees the accuracy of the diagnosis at the morphological level. In endoscopic and morphological studies, it was found that most stomach ulcers are located in the area of the lesser curvature and antrum, much less often - on the greater curvature and in the area of the pyloric canal. 90% of duodenal ulcers are located in the bulbar region. A peptic ulcer is typically round or oval in shape. Its bottom consists of necrotic masses, under which there is granulation tissue. The presence of dark blotches on the bottom indicates bleeding. The ulcer healing phase is characterized by a decrease in hyperemia of the mucous membrane and an inflammatory shaft in the periulcerous zone. The defect becomes less deep, gradually cleared of fibrinous plaque. The scar looks like a hyperemic area of the mucous membrane with linear or stellate retractions of the wall. In the future, during endoscopic examination at the site of the former ulcer, various violations of the relief of the mucous membrane are determined: deformations, scars, narrowing. At endoscopy, a mature scar due to the replacement of a defect with granulation tissue has a whitish appearance, there are no signs of active inflammation. A morphological study of a biopsy specimen obtained from the bottom and edges of the ulcer reveals cellular detritus in the form of an accumulation of mucus with an admixture of decaying leukocytes, erythrocytes and desquamated epithelial cells with collagen fibers located underneath. Differential diagnostics. With the widespread use of endoscopy, the differential diagnosis of ulcerations of the stomach and duodenum (symptomatic ulcers, specific ulcerations in tuberculosis, syphilis, Crohn's disease, primary ulcerative cancer, secondary malignant ulcers) becomes especially important. For symptomatic ulcers, there must be a cause that caused them (extreme exposure, clinical and morphological signs of endocrine diseases, cardiovascular and respiratory disorders, rheumatic diseases). More than for peptic ulcer, they are characterized by a multiplicity of lesions, predominant localization in the stomach, and significant size. With peptic ulcer, pain syndrome prevails, and with chronic gastritis - dyspeptic phenomena. In chronic gastritis, pain is mild or absent, there is no seasonality of the disease and limited pain on palpation; the aggravation of the disease often depends on the nature of the food. The state of the secretory function of the stomach with gastritis can be different. Of decisive importance are gastroscopy and gastrobiopsy, in which mucosal changes characteristic of gastritis and an ulcer in peptic ulcer are detected. Hiatus hernia (HH) is also often accompanied by pain in the epigastrium. However, unlike peptic ulcer disease, this disease is characterized mainly by the elderly age of patients, the relationship of pain with the position of the body (pain increases in the supine position, weakens in the upright position). The diagnosis of HH is confirmed by the results of X-ray examination. Chronic cholecystitis is characterized by pain in the right hypochondrium and epigastrium, often radiating to the right shoulder blade, to the shoulder, to the angle of the lower jaw on the right. With acalculous cholecystitis, they have a dull, monotonous, pressing character, and with calculous cholecystitis, they acquire the character of colic. Nausea, constipation, flatulence are noted. Persistent subfebrile condition is possible. With prolonged obstruction of the bile ducts, jaundice may join. The diagnosis of damage to the biliary system is verified by the data of abdominal ultrasound, X-ray examination (cholecystography), endoscopic retrograde cholepancreatography (ERCP), as well as the results of duodenal sounding, which is indicated only for a stoneless process. In acute pancreatitis and exacerbation of chronic pain, they are localized in the left half of the epigastric region, are shingles in nature, provoked by the intake of any food. In the anamnesis - pathology of the biliary system, alcohol abuse, long-term use of pancreatic drugs. Objectively reveal weight loss, polyfecal, steatorrhea, creatorrhea. The diagnosis is confirmed by the results of a biochemical blood test for pancreatic enzymes, feces - for digestibility, as well as instrumental data. Treatment. Rational therapy for peptic ulcers should include a regimen, appropriate nutrition, drug treatment, psychotherapy, physical and spa treatment methods. During the period of exacerbation of peptic ulcer disease, it is necessary to strictly observe a fractional diet (from 4 to 6 times a day with a small volume of each portion of food taken at certain hours). Food products must have good buffering properties and contain sufficient protein (120–140 g). Psychotherapy is essential for stopping or reducing psychoneurotic reactions arising from persistent pain syndrome and its expectation. Medicines used to treat peptic ulcers are divided into 5 groups: 1) drugs that affect the acid-peptic factor (antacids and H2histamine blockers, other antisecretory agents); 2) drugs that improve the gastric mucosal barrier; 3) drugs that increase the synthesis of endogenous prostaglandins; 4) antibacterial and antiseptic agents; 5) drugs that normalize motor-evacuation disorders of the stomach and duodenum. Antacids: 1) soluble (absorbable) - bicarbonate of soda, calcium carbonate (chalk) and magnesium oxide (burnt magnesia); 2) insoluble (non-absorbable): magnesium trisilicate and aluminum hydroxide. Soluble antacids have a fast, energetic, but short-term alkalizing effect, but often cause side effects, which is why they are not used in the treatment of peptic ulcers. Insoluble antacids based on aluminum hydroxide and magnesium hydroxide (Almagel, Phosphalugel, Gelusillac, Topaal, Maalox, etc.) provide long-term neutralization of hydrochloric acid, envelop the mucous membrane, protecting it from the damaging effects of acid and food. In addition to neutralizing hydrochloric acid, they help reduce the proteolytic activity of gastric juice, bind lysolecithin and bile acids, and have a universal cytoprotective effect. Antacids should be taken 1-2 hours after meals and at night. Maalox is prescribed in suspension (15 ml 4 times a day) or tablets (1-2 tablets 4 times a day), phosphalugel - in the form of a gel (16 g 3-4 times a day). One of the main side effects of nonabsorbable antacids is stool disturbance. Aluminum hydroxide preparations cause constipation, and magnesium hydroxide preparations (Maalox) have a dose-dependent laxative effect. A new era in the treatment of peptic ulcer began with the advent of H2- histamine blockers. Under physiological conditions, histamine mediates extragastric nerve and humoral stimuli that cause acid production. Stimulation of the production of hydrochloric acid by histamine is due to an increase in the activity of cAMP, which acts on the enzyme adenylcyclase contained in the acid-producing region of the stomach, which enhances the secretion of hydrogen ions. The data obtained were the basis for the synthesis of drugs that interrupt the participation of histamine in the secretory process at the cellular level, such as cimetidine, ranitidine, famotidine, nizatidine, etc. In addition, H antagonists2Histamine receptors prevent microcirculation disorders in the gastric mucosa and thus prevent the development of ulcers. In addition, they reduce the production of pepsin, increase the secretion of bicarbonates, normalize gastroduodenal motility, increase the number of DNA-synthesizing epithelial cells, stimulating reparative processes and accelerating the healing of chronic gastric and duodenal ulcers. However, 1st generation drugs (cimetidine, cinamet, belomet, tagamet) can cause changes in the nervous system, toxic hepatitis, rhythm and conduction disturbances in the cardiovascular system, and changes in the hematopoietic organs. H blockers2subsequent generations of histamine receptors - ranitidine (zantak, ranisan, gistak), famotidine (kvamatel, lecedil, gastrosidin), nizatidine (roxatidine) differ from cimetidine in good tolerance. Ranitidine is prescribed at a dose of 150 mg 2 times a day, famotidine - 20 mg 2 times a day for 4-6 weeks. To prevent withdrawal syndrome after ulcer healing, it is recommended to continue taking ranitidine (150 mg) or famotidine (20 mg) at night for 2-3 months. In recent years, a new antisecretory drug omeprazole (omenrol, omez, losek), which belongs to benzimidazole derivatives, has appeared. It blocks the enzyme H + -K + -ATPase of the proton pump of the parietal cell. The short half-life (about 1 hour) and long duration of action (18-24 hours) make it possible to take this drug once. Omeprazole is prescribed 20 mg at night 1 time per day for 2-3 weeks. Omeprazole ranks first in terms of the severity of the antisecretory effect among modern antiulcer drugs. Side effects of the drug are not very pronounced. Widespread use in the treatment of peptic ulcers has found gastrocepin (nirenzepine, gastrozepine), which belongs to anticholinergic drugs. The drug selectively blocks muscarinic acetylcholine receptors located in the cells of the gastric mucosa that produce hydrochloric acid and pepsin. Gastrocepin has an inhibitory effect on basal and stimulated gastric secretion, inhibits the production of pepsin, slows down evacuation from the stomach, causes inhibition of gastrin production, reduces the level of pancreatic polypeptide, has a cytoprotective effect by increasing the production of gastric mucus glycoproteins, as well as by improving the blood supply to the mucous membrane of the gastroduodenal region . Assign it to 50 mg 2 times a day 30 minutes before meals. The course of treatment is an average of 4 weeks. Medicines that strengthen the mucous barrier of the stomach include preparations of colloidal bismuth (denol), which forms a protective film on the mucous membrane, reduces the peptic activity of the stomach, forming an insoluble compound with pepsin, enhances mucus formation, has a cytoprotective effect, increasing the content of prostaglandins in the stomach wall. Denol has the ability to inhibit the activity of HP in the gastric mucosa. The drug is prescribed 2 tablets (240 mg) 2 times a day half an hour before meals or 2 hours after meals. To avoid the accumulation of bismuth salts in the body, it is not recommended to carry out therapy with these drugs for more than 8 weeks. For the purpose of antibacterial therapy for gastric and duodenal ulcers, tetracycline, amoxicillin, and clarithromycin are used. They are used in combination with other antiulcer drugs. Several schemes of combination therapy (two-, three-, four-component) have been proposed. Two-component therapy: amoxicillin 1000 mg 2 times a day for 2 weeks; omeprazole 40 mg twice a day. The three-component scheme includes the preparation of colloidal bismuth 2 mg 120 times a day; tetracycline 4 mg 250 times a day; metronidazole 4 mg 250 times a day. The therapy cycle is 4 days. The four-component scheme involves omeprazole 20 mg 2 times a day from the 1st to the 10th day; de-nol 120 mg 4 times a day from the 4th to the 10th day; tetracycline 500 mg 4 times a day from the 4th to the 10th day; metronidazole 500 mg 3 times a day from the 4th to the 10th day. The four-component scheme for the treatment of peptic ulcer of the stomach and duodenum is recognized as the most effective. 6 weeks after it, the healing of the peptic defect is observed in 93-96% of patients. After scarring of a peptic ulcer of the stomach and duodenum, two types of treatment are traditionally used. 1) Continuous maintenance therapy is carried out with antisecretory drugs at half the daily dose for a period of up to one year. 2) Therapy "on demand", involves the use of one of the antisecretory agents in half the daily dose for two weeks when symptoms of peptic ulcer appear. Prognosis and prevention. Uncomplicated forms of the disease have a favorable prognosis for life and work. In case of complications of peptic ulcer disease, the prognosis is determined by the timeliness of surgical care. Prevention of peptic ulcer recurrence includes dynamic monitoring with mandatory follow-up examinations by a doctor 2 times a year. Examinations should include clinical and endoscopic, and, if necessary, morphological examination. As a preventive measure, it is recommended to normalize sleep and rest, give up bad habits, limit the intake of ulcerogenic medications, rational five meals a day and use two- or three-component therapy for a week every 3 months. Author: Mostovaya O.S. << Back: Diseases of the digestive tract. Diseases of the stomach. Chronic gastritis
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