Ulcer disease. Nursing care for peptic ulcer presentation for a lesson on the topic Peptic ulcer of the stomach and 12 duodenal ulcer presentation


  • Donetsk national medical
  • university. M. Gorky
  • Department of Surgery. K.T. Hovnatanyan
  • Assoc. Dudin A.M.
Peptic ulcer of the stomach and 12p. intestines - one of the main problems of gastroenterology.
  • Peptic ulcer of the stomach and 12p. intestines - one of the main problems of gastroenterology.
  • The disease of the 21st century is an increase in the load, the requirements for a person, his psyche, frequent stressful situations, malnutrition.
  • Up to 5 cases of peptic ulcer are registered per 1000 population.
  • Ulcers in 12p. intestine are found 5-10 times more often than in the stomach.
  • Women get sick less often than men.
The stomach and duodenum are frequent objects of surgical interventions that surgeons have to perform in different conditions. The stomach is located in the epigastric region, its capacity is up to 2 liters.
  • The stomach and duodenum are frequent objects of surgical interventions that surgeons have to perform in different conditions. The stomach is located in the epigastric region, its capacity is up to 2 liters.
  • Sections of the stomach: cardia, fundus, body, antrum, pylorus. The wall of the stomach consists of serous, muscular, submucosal and mucous membranes.
  • The serous membrane, passing to neighboring organs, forms a ligamentous apparatus:
  • phrenic-gastric ligament
  • hepatogastric ligament (small omentum)
  • gastro-splenic ligament
  • gastrocolic ligament
  • gastro-pancreatic ligament
Blood supply - branches of the celiac trunk of the aorta - the left gastric artery, hepatic and splenic. Venous blood flows into the portal vein system.
  • Blood supply - branches of the celiac trunk of the aorta - the left gastric artery, hepatic and splenic. Venous blood flows into the portal vein system.
  • The stomach is innervated by sympathetic and parasympathetic fibers. Sympathetic nerves branch off from the solar plexus to the stomach. Parasympathetic innervation - vagus nerves.
In the stomach, food is chemically processed and portionwise evacuated to the intestines.
  • In the stomach, food is chemically processed and portionwise evacuated to the intestines.
  • In addition, it produces an internal factor - gastromucoprotein, which plays an important role in hematopoiesis.
  • Food is processed with hydrochloric acid and pepsin, which are formed from pepsinogen.
  • Hydrochloric acid - parietal cells. Pepsinogen are chief cells.
Main and additional etiological factors:
  • Main and additional etiological factors:
  • Main: the presence of H. Pylori
  • Additional - psychological trauma, experiences, trauma to the brain, nervous system, eating disorders, gastritis, smoking, heredity.
Morphologically, peptic ulcer of the stomach and intestines is characterized by the presence of erosions, acute or chronic ulcers.
  • Morphologically, peptic ulcer of the stomach and intestines is characterized by the presence of erosions, acute or chronic ulcers.
  • Erosion is a superficial mucosal defect.
  • Acute ulcer - a defect no deeper than the submucosal layer from 2-3 mm to 2-3 cm in diameter.
  • Chronic ulcer - proliferation of connective tissue, inflammatory infiltration at the edges and at the bottom of the ulcer. In advanced cases - dense, callused edges and bottom (calles ulcer).
  • penetration
  • Perforation
  • Bleeding
  • Malignization
  • Stenosis of the lumen with impaired evacuation
As you know, the main complaints of patients with peptic ulcer are pain (92%), heartburn (50%), vomiting (64%), nausea (50%), belching (24%).
  • As you know, the main complaints of patients with peptic ulcer are pain (92%), heartburn (50%), vomiting (64%), nausea (50%), belching (24%).
  • The clinic of peptic ulcer disease has its own characteristics depending on the localization of the ulcer, gender, age of the patient, and the presence of complications.
  • With peptic ulcer, the secretory function of the stomach is usually increased, hyperacidity is noted.
Cardia ulcers account for 6-8%
  • Cardia ulcers account for 6-8%
  • Ulcers of greater curvature are less common and usually malignant. Often penetrate into the omentum, mesentery, spleen, pancreas.
  • Pyloric ulcers - from 2 to 7% of cases. They rarely perforate, but often bleed.
  • Ulcers 12p of the intestine in 85% are located at a distance of 2 cm from the pylorus, in 10% - 5 cm, in 5% - more than 5 cm from the pylorus.
  • Extrabulbous or postbulbar ulcers occur in 5-20% of cases. These ulcers often give bleeding, early stenosis.
  • Giant ulcers (more than 3 cm in diameter) can be localized both in the stomach and in the 12th intestine.
  • Direct and indirect signs.
  • Direct: "niche", inflammatory shaft, convergence of folds. "Niche" is an additional shadow or pathological protrusion of the contour of the stomach, the most reliable sign of an ulcer.
  • Indirect signs: spastic phenomena, changes in peristalsis, impaired motility of the stomach, changes in tone, mucosal relief.
  • In the 12th duodenum, ulcers are sometimes revealed that oppose each other ("kissing" or "mirror").
  • Before the advent of fiberoptic endoscopes, the main method of diagnosing ulcers was radiography.
Ulcer of the lesser curvature of the body of the stomach
  • In 1958 Girshovich proposed a fiberscope with fiber optics.
  • From this point on, gastroduodenoscopy is the main one in the diagnosis of peptic ulcer.
Fibrogastroduodenoscopy
  • often accompanied by severe pain with vomiting. Hyperacidity! Early manifestation of combined complications, perforation of "silent" ulcers.
  • proceeds without the expressed pain syndrome. Often hypoacidity! In 63% of cases, they are localized in the stomach, bleed, malignant.
  • Absolute - perforation, stenosis, suspicion of malignancy of a gastric ulcer, unstoppable bleeding.
  • Relative indications are callous ulcers, penetrating, pyloric ulcers of the greater curvature and posterior wall, cardia, failure of conservative treatment.
The first resection of the stomach for cancer of the outlet section was performed in 1879 by the French surgeon Pean. The patient died on the 4th day, no autopsy was performed.
  • The first resection of the stomach for cancer of the outlet section was performed in 1879 by the French surgeon Pean. The patient died on the 4th day, no autopsy was performed.
  • The first successful resection of the stomach was made in 1881 in Vienna by Theodor Billroth (1 method). In 1885 - Billroth II.
  • In Russia, the first resection of the stomach was performed by Kitaevsky in 1881. In 1906, Kronlein declared gastroenterostomy the operation of choice for peptic ulcer disease. In the 1930s, HEA was widely used, then less frequently due to peptic ulcers.
  • anterior collateral - posterior and anterior
  • retrocolic - posterior and anterior
1.Resection of the stomach
  • 1.Resection of the stomach
  • Distal resection 2/3 - 3/4 according to B-1
  • Distal resection 2/3 - 3/4 according to B-2
  • 2. Vagotomy with drainage operation
  • Trunk vagotomy with hydroelectric power station
  • Stem vagotomy with pyloroplasty
  • Stem vagotomy with GDS
  • Selective vagotomy with pyloroplasty, GDS
  • 3. Vagotomy with resection of the stomach according to B-1 in various modifications, incl. with the preservation of the gatekeeper
functional bed
  • functional bed
  • Observation (pulse, temperature, blood pressure, respiratory rate, red blood)
  • Humidified O2
  • Banks, mustard plasters
  • exercise therapy, massage
  • Alkaline inhalations.
  • Probe power according to the scheme
  • Aspiration of stomach contents according to indications.
  • Pain relief (drugs, analgesics).
  • Antibacterial therapy
  • Stimulation of the respiratory center (cordiamin)
  • IV detoxification (glucose, gemodez)
  • Parenteral nutrition (Lipofundin, Alvezin)
  • Correction of water and electrolyte disorders (R-r Fox, Ringer)
  • Dressings
  • Active methods of detoxification (blood UVI, ILBI, plasmapheresis)
  • Fight against intestinal paresis (prozerin, cerucal, kalimin, intravenous 10% NaCl, hypertonic enemas, epidural anesthesia).
Group 1: early complications (failure of anastomotic sutures, intestinal stump, bile duct injury, bleeding into the abdominal cavity, into the organ, pancreatitis, peritonitis, intestinal obstruction, pulmonary atelectasis, pneumonia, thromboembolism)
  • Group 1: early complications (failure of anastomotic sutures, intestinal stump, bile duct injury, bleeding into the abdominal cavity, into the organ, pancreatitis, peritonitis, intestinal obstruction, pulmonary atelectasis, pneumonia, thromboembolism)
  • Group 2: late (gastrointestinal ulcers, obstruction of the anastomosis, hernia, adhesive disease).
Grossius (1695) was the first to report a perforated gastric ulcer.
  • Grossius (1695) was the first to report a perforated gastric ulcer.
  • Surgical treatment of this complication began to develop in the late 19th century.
  • Mikulich in 1880 Performed the first suturing of a perforated ulcer.
  • In Russia, this operation was first carried out by Vanakh in 1897.
  • According to the literature, the frequency of perforations ranges from 3 to 30%. 55% of perforations are ulcers of the 12th intestinal tract, 25% - ulcers of the lesser curvature of the stomach and 20% - of the prepyloric region.
Mondor (1938) divided all signs of a perforated ulcer into 2 groups:
  • Mondor (1938) divided all signs of a perforated ulcer into 2 groups:
  • The main symptoms are pain, tension in the muscles of the abdominal wall, ulcer history. Sudden sharp pain in the abdomen (“stab”) is the leading sign of a perforated ulcer.
  • Adverse symptoms are divided into functional, physical and general.
  • Functional signs according to Mondor: vomiting, retention of stools, gases and intense thirst.
  • Physical signs are found during examination, palpation, percussion, auscultation (forced position with knees adducted, avoiding the slightest movement. Shchetkin-Blumberg symptom is positive, hyperesthesia of the abdominal skin).
  • The tension of the muscles of the abdominal wall is the first symptom that the doctor finds on palpation, the so-called board-shaped abdomen. In some patients, there is no ulcerative history - "silent" perforation (2-3%).
Bernstein (1947) described a genital symptom in men - the testicles are pulled up to the external opening of the inguinal canal, the skin of the scrotum is as if corrugated, the penis is turned upside down.
  • Bernstein (1947) described a genital symptom in men - the testicles are pulled up to the external opening of the inguinal canal, the skin of the scrotum is as if corrugated, the penis is turned upside down.
  • In 86% of cases, a symptom of the disappearance of hepatic dullness is determined (Clark's s-m)
  • On rectal examination, pain in the area of ​​the Douglas space (p. Kulenkampf).
  • General signs are the state of the pulse, respiration, temperature, the pulse is first brady -, then tachycardia. Breathing is shallow, labored.
There are three periods during a perforated ulcer:
  • There are three periods during a perforated ulcer:
  • Shock period (6-8 hours)
  • The period of imaginary well-being (8-10 hours)
  • Period of progressive peritonitis
Covered perforation (perforatio tecta) was first described in 1912. Schnitzler
  • Covered perforation (perforatio tecta) was first described in 1912. Schnitzler
  • Occurs in 5-8% of cases. Diagnosis is difficult, because a small amount of gas and liquid enters the abdominal cavity
  • Ratner-Vicker symptom is characteristic (long-term persistent muscle tension in the right upper quadrant of the abdomen with a general good condition of the patient)
  • Covered perforation
X-ray examination in the diagnosis of perforated ulcers is a valuable help!
  • X-ray examination in the diagnosis of perforated ulcers is a valuable help!
  • Revealed pneumoperitoneum on the survey x-ray in the form of a sickle-shaped strip of gas under the diaphragm.
  • In some cases, pneumogastrography is used (200-500 ml of air is injected through a thin gastric tube, then pictures are taken)
  • A very valuable method is laparoscopy.
Perforated ulcer (pneumoperitoneum) Diff. diagnosis - acute cholecystitis, intestinal obstruction, acute pancreatitis, renal colic, acute appendicitis, ischemic heart disease
  • Dif. diagnosis - acute cholecystitis, intestinal obstruction, acute pancreatitis, renal colic, acute appendicitis, ischemic heart disease
  • Should be the law - if perforation is suspected - urgent laparotomy or laparoscopy.
  • Differential Diagnosis
Shaving the surgical field
  • Shaving the surgical field
  • Cleansing enemas, siphon
  • Aspiration of stomach contents
  • If necessary - infusion therapy with appropriate drugs for 2 hours
  • If possible - the study of biochemical parameters of blood, ECG
  • Preparing for the operation
The main method is operation. More than 30 methods of treatment are known. The most commonly used is a simple suturing of the perforated hole, closing the hole with an omentum on the leg. Primary resection of the stomach - up to 6 hours prescription of perforation. The most correct is excision of the ulcer with pyloroplasty.
  • The main method is operation. More than 30 methods of treatment are known. The most commonly used is a simple suturing of the perforated hole, closing the hole with an omentum on the leg. Primary resection of the stomach - up to 6 hours prescription of perforation. The most correct is excision of the ulcer with pyloroplasty.
  • Anesthesia - endotracheal anesthesia.
  • The sequence of the operation is revision, suturing the hole, sanitation of the abdominal cavity, drainage at 4 points with tubes. In our opinion, the combination of stem vagotomy with excision of the ulcer and pyloroplasty according to Judd is the most appropriate. Be sure to complete pyloroplasty with a feeding probe.
  • Peritoneal dialysis - in case of purulent peritonitis.
  • Treatment of a perforated ulcer
They are observed in many diseases and it is often very difficult to recognize their cause. Common to all patients in such cases is the need to provide them with emergency care.
  • They are observed in many diseases and it is often very difficult to recognize their cause. Common to all patients in such cases is the need to provide them with emergency care.
  • The first information about bleeding is given by Avicena (X century). The first resection of the stomach for a peptic ulcer complicated by bleeding was performed by Ridiger in 1881. Further development of surgery for acute gastrointestinal bleeding is associated with the names of Spasokukotsky, Finsterer, Yudin, Berezov, Rozanov, Shalimov.
Patients with gastrointestinal bleeding can be divided into 2 large groups according to the causes of their occurrence:
  • Patients with gastrointestinal bleeding can be divided into 2 large groups according to the causes of their occurrence:
  • Group 1 - patients with pathological processes in the stomach and intestines, primarily as a complication of peptic ulcer. According to various authors, bleeding occurs in 4-26% of patients suffering from this pathology. This group also includes bleeding that occurs with polyposis of the stomach, the collapse of a cancerous tumor of the stomach, infringement of the stomach wall with a hernia of the esophageal opening of the diaphragm, with Mallory-Weiss syndrome, bleeding from varicose veins of the esophagus with portal hypertension (liver cirrhosis, thrombophlebitis, splenomegaly, tumors and inflammatory diseases of the pancreas).
  • Group 2 - patients suffering from hypertension, hemorrhagic diathesis, leukemia, Werlhof's disease, Shenlein-Genoch's disease, radiation sickness, beriberi, etc.
The main classification of bleeding is clinical symptoms.
  • The main classification of bleeding is clinical symptoms.
  • blood loss up to 20% of the BCC is considered average,
  • over 20% - large or massive.
  • The 1st degree is mild and is observed with blood loss up to 20% of the BCC (up to 1 liter per 70 kg of body weight). The general condition is satisfactory or moderate, pallor. Sweating, R-90 -100 bpm, BP - 100-90/60 mm Hg st. Consciousness is clear, breathing is slightly accelerated. Reduced urination. Without compensation for blood loss, the patient will survive.
  • 2nd degree - moderate. Blood loss from 20 to 30% of the BCC (from 1 to 1.5 liters per 70 kg of body weight). The state of moderate severity, the patient is lethargic, speaks slowly, quietly. Pallor of the skin, sticky sweat, P - 100-120 per minute, weak filling, blood pressure 90-80/50 mm Hg, rapid shallow breathing, oliguria are expressed.
  • Without compensation for blood loss, the patient can survive, however, with significant disorders of blood circulation, metabolism and the function of some organs, especially the kidneys, liver, and intestines.
  • According to A.A. Shalimov allocate 3 degrees of blood loss
3rd degree - a serious condition, observed with blood loss from 30 to 50% of the BCC (from 1.5 to 2.5 liters per 70 kg of body weight). The condition is severe or extremely severe, inhibition of the motor reaction, the skin and mucous membranes are pale cyanotic. The patient answers questions slowly, in a whisper, partially loses consciousness. P is filiform, 130-140 per minute, systolic blood pressure is 70-50 mm Hg, diastolic is not detected. Breathing is shallow, infrequent. Body, limbs cold. Burstein's sign appears. When pressing on the limb, a slowly disappearing white spot is formed. Oliguria is replaced by anuria. Often there are hemorrhagic phenomena indicating widespread intravascular thrombosis - DIC.
  • 3rd degree - a serious condition, observed with blood loss from 30 to 50% of the BCC (from 1.5 to 2.5 liters per 70 kg of body weight). The condition is severe or extremely severe, inhibition of the motor reaction, the skin and mucous membranes are pale cyanotic. The patient answers questions slowly, in a whisper, partially loses consciousness. P is filiform, 130-140 per minute, systolic blood pressure is 70-50 mm Hg, diastolic is not detected. Breathing is shallow, infrequent. Body, limbs cold. Burstein's sign appears. When pressing on the limb, a slowly disappearing white spot is formed. Oliguria is replaced by anuria. Often there are hemorrhagic phenomena indicating widespread intravascular thrombosis - DIC.
  • Without timely compensation for blood loss, patients die from the death of cells of the gastrointestinal tract, liver, kidneys, and a decrease in cardiac activity.
  • According to A.A. Shalimov allocate 3 degrees of blood loss
Blood loss of 50-60% of BCC leads to rapid death of the body from cardiac arrest.
  • Blood loss of 50-60% of BCC leads to rapid death of the body from cardiac arrest.
  • According to A.A. Shalimov allocate 3 degrees of blood loss
The clinical picture of gastrointestinal bleeding basically does not depend on the etiology, but is directly dependent on the amount of blood lost.
  • The clinical picture of gastrointestinal bleeding basically does not depend on the etiology, but is directly dependent on the amount of blood lost.
  • General weakness, dizziness, pallor of the skin, increased heart rate are characteristic of these patients.
  • In some cases, collapse may occur, the patient loses consciousness, the skin is waxy, cold sweat, the pupils dilate, the threadlike pulse is not counted.
  • A/D and R data are not always adequate to the degree of blood loss. The study of red blood must be carried out in dynamics, be sure to monitor the hematocrit. So with the loss of 500 ml of blood, Ht is within 40-44, up to 1 liter - 32-38.
  • The most reliable data on the amount of blood loss can be obtained by determining the BCC and its components.
gastroduodenal bleeding presents a difficult issue.
  • gastroduodenal bleeding presents a difficult issue.
  • History plays a big role.
  • Ulcerative bleeding is often preceded by increased pain, which disappears after the onset of bleeding (Bergman's report) in 84% of cases.
  • The nature of hematemesis is an important diagnostic feature. So, vomiting of scarlet blood with clots, as a rule, is a sign of bleeding from the esophagus.
  • The presence of "coffee grounds" indicates hemorrhage from the stomach or 12th intestine. When a large amount of blood enters the intestine, peristalsis increases, which can be determined by auscultation (sim. Taylor).
  • Rectal examination is important. The presence of melena is a 100% sign of bleeding. If scarlet fresh blood is found on the glove, one should think about bleeding from the rectum, sigma.
  • To date, the main method for diagnosing gastroduodenal bleeding is fibrogastroduodenoscopy.
Quoting a phrase from the monograph by V.S. Rozanov on bleeding, we remember the following: for all non-ulcer bleeding, regardless of age, degree of anemia and frequency of bleeding, conservative treatment is indicated.
  • Quoting a phrase from the monograph by V.S. Rozanov on bleeding, we remember the following: for all non-ulcer bleeding, regardless of age, degree of anemia and frequency of bleeding, conservative treatment is indicated.
  • With ulcerative bleeding, the threat to life is so great that it is necessary to raise the question of early surgical intervention.
  • It must be remembered that treatment tactics should be determined strictly individually.
  • After stopping the bleeding - the Meilengracht diet - tea, white bread, sour cream, scrambled eggs, mashed potatoes, jelly, butter.
  • After determining the group and Rh affiliation of blood, a single-group erythrocyte mass of early storage periods is transfused to compensate for the deficiency. They are poured more often into / in a drip, but sometimes in a jet into several veins.
  • In/venous native or dry plasma (400-600 ml), polyglucin up to 400, 5-10% albumin solution 200 ml
  • Direct blood transfusions are now officially prohibited.
  • Replenishment of the BCC should be carried out under the control of the CVP (70-150 mm of water.st)
  • Transfusion of fibrinogen up to 5 g per day with aminocaproic acid 5% - 200-300 ml
  • Ascorbic acid 5% - 10-20 ml
  • Pituitrin 20 units (4 ml) IV drip, 5% - 500 ml glucose
  • Vikasol 5ml IV drip
  • B vitamins
  • A mandatory measure is the supply of humidified O2
  • Calcium chloride or gluconate 10%-10.0 IV
  • A modern and effective method for the treatment of bleeding ulcers is FGDS with possible diathermocoagulation or laser hemostasis, adhesive application.
Various methods of operation are used.
  • Various methods of operations are used.
  • At the height of bleeding in sharply weakened patients with a high operational risk, gastrotomy, wedge-shaped excision or suturing of the bleeding vessel with non-absorbable sutures is performed.
  • When bleeding from an ulcer 12p. intestines - duodenotomy and flashing of the vessel are supplemented with 2-sided stem vagotomy.
  • With relative compensation in patients with ulcer 12p. intestines perform one of the varieties of vagotomy, duodenotomy with excision or sheathing of the ulcer with non-absorbable sutures, followed by pyloroplasty.
  • Gastric resection is performed for gastric ulcers and very large penetrating ulcers 12p. intestines in a relatively satisfactory condition of the patient. In no case should you perform a resection of the stomach for "off".
  • reduces blood flow in the mucosa, promoting hemostasis
  • on the other hand, it reduces acidity, creating conditions for the healing of ulcers.
  • Positive aspects of vagotomy
Penetration of stomach ulcers and 12p. intestines is a kind of perforation and is characterized by a slow gradual course.
  • Penetration of stomach ulcers and 12p. intestines is a kind of perforation and is characterized by a slow gradual course.
  • Most often, a stomach ulcer penetrates into the lesser omentum, pancreas, liver, colon, and its mesentery. Ulcer 12p. intestines usually penetrates into the pancreas, hepato-12-duodenal ligament, less often into the gallbladder with the formation of an internal fistula.
  • Characteristic symptoms of ulcer penetration are back pain, severe night pain, change in the previous nature of the pain, their constant nature, despite vigorous treatment.
Choledochoduodenal fistula Pyloric stenosis occurs as a result of scarring of the ulcer of the pyloroduodenal zone. There are 3 clinical stages of pyloric stenosis:
  • Pyloric stenosis occurs as a result of scarring of the ulcer of the pyloroduodenal zone. There are 3 clinical stages of pyloric stenosis:
  • Compensated stenosis - a constant feeling of heaviness in the epigastrium, periodically vomiting of gastric contents. On an empty stomach in the stomach 200-300 ml of liquid.
  • Subcompensated stenosis - the same + 2-3 r. On the day of vomiting up to 0.5 liters or more with an admixture of food. Emaciation.
  • Decompensation - the above phenomena progress rapidly. The patient is exhausted, dehydrated. In the epigastrium "splashing noise". Visually, percussion can determine the contours of the overdistended stomach. Vomiting of eaten food with a rotten smell. Electrolyte imbalances can lead to gastric tetany with seizures and psychosis (achlorhydria).
Decompensated pyloric stenosis (12 hours after barium administration) Decompensated pyloric stenosis (24 hours after barium administration) One of the features of gastric ulcer that distinguishes it from peptic ulcer 12p. intestines, is the possibility of malignant degeneration of gastric ulcers. In the literature, there are only single observations of cancer that arose from a 12p ulcer. intestines.
  • One of the features of gastric ulcer, which distinguishes it from peptic ulcer 12p. intestines, is the possibility of malignant degeneration of gastric ulcers. In the literature, there are only single observations of cancer that arose from a 12p ulcer. intestines.
  • For the first time proved the possibility of stomach cancer at the site of an ulcer, Zenker's student, Hauser (1883). He came to the following conclusions: 1. From chronic, especially large, stomach ulcers, cancer can occur. 2. In the initial stages, malignancy occurs in the mucosa of the edge of the ulcer. 3. Atypical proliferation of the epithelium of the glands progresses and takes on the character of malignant growth.
  • According to various authors, an ulcer turns into cancer in 8-18.5% of cases.
Cancer ex ulcere, when cancer develops from the edge of a stomach ulcer
  • Cancer ex ulcere, when cancer develops from the edge of a stomach ulcer
  • Cancer ulcerative, when malignancy develops at the bottom of an ulcer
  • Cancer ex cicatrix, i.e. cancer that develops at the site of the scar of a healed ulcer
  • Histologically, adenocarcinoma is most commonly found.
Unfortunately, there is not a single unmistakable clinical criterion for recognizing the early stages of malignant degeneration of a chronic gastric ulcer.
  • Unfortunately, there is not a single unmistakable clinical criterion for recognizing the early stages of malignant degeneration of a chronic gastric ulcer.
  • It is recommended to use such clinical symptoms as deterioration in general condition, loss of appetite, aversion to meat food, decreased acidity, the appearance of lactic acid in gastric juice.
  • Light intervals during the course of the disease are reduced, or completely disappear. Compliance with diet and rest does not work.
  • Drug treatment, which previously eliminated various dyspeptic disorders, becomes ineffective. Vomiting appears, the patient loses weight.
  • The criterion for degeneration is the localization of the ulcer and its size.
Ulcers of the pyloric antrum and lesser curvature at the angle of the stomach (mostly benign)
  • Ulcers of the pyloric antrum and lesser curvature at the angle of the stomach (mostly benign)
  • Cardiac, subcardiac, anterior and posterior wall (more often malignant)
  • Ulcers of greater curvature (almost always malignant)
  • Summarizing the literature data, it can be noted that ulcers of the greater curvature are malignant in 90% of cases, ulcers in the lower third of the stomach - in 80%, in / 3 of the lesser curvature in 48%
  • It is impossible to use the localization and size of the ulcer as an absolute differential diagnostic sign; it is imperative to use a histological examination of the ulcer by biopsy through a fibrogastroscope at 5 points (polypositional biopsy).
  • Of the laboratory diagnostic methods, the most important is the cytological examination of gastric lavage.
  • X-ray diagnosis of benign and malignant gastric ulcers in the early stages is very difficult.
Cancer of the antrum
  • In summary, active management is recommended for gastric ulcers.
  • In the most vivid and concise form, the great surgeon S.S. expressed his attitude to the treatment of stomach ulcers. Yudin: “the larger the ulcer, the deeper the “niche”, the older the patient, the lower the acidity, the greater the risk of cancer from the ulcer, and therefore, the sooner gastric resection is indicated.”
The choice of surgical intervention for malignant ulcers of the middle and n / 3 of the stomach should be considered subtotal resection of the stomach with lesser and greater omentum and regional lymph nodes.
  • The choice of surgical intervention for malignant ulcers of the middle and n / 3 of the stomach should be considered subtotal resection of the stomach with lesser and greater omentum and regional lymph nodes.
  • With high ulcers, subtotal proximal resection of the stomach is indicated, with multiple ulcers - gastrectomy with removal of omentums and regional l / nodes.
  • The prognosis for malignant ulcers is better than for primary gastric cancer.
  • Only early surgical treatment can significantly improve the results of the treatment of chronic ulcers, and hence cancer arising from the ulcer.

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Description of the presentation Presentation Modern methods of diagnosis and surgical treatment of gastric ulcer and 12-p according to slides

Saratov State Medical University Department of Hospital Surgery, Faculty of Medicine. Head Honored Worker of Science of the Russian Federation, Professor R. Z. Losev. Modern methods of diagnosis and surgical treatment of gastric ulcer and duodenal ulcer.

Peptic ulcer (PU). Concept definition. PU is a chronic relapsing disease characterized by the formation of a persistent defect in the mucous membrane of the stomach or duodenum due to a disorder of the general and local mechanisms of the nervous, hormonal, immune regulation, the main functions of the gastroduodenal system, trophic disorders and the development of proteolysis in the mucous layer.

Predisposing factors 1. 1. Heredity 2. 2. Prolonged psycho-emotional stress 3. 3. Dietary errors 4. 4. Bad habits (alcohol, smoking) hypotheses. I WOULD. Etiology and pathogenesis

1. 1. Vascular theory (R. Virchow) Anatomical changes in the vessels in the ulcer zone (thrombosis, embolism, stenosis) 2. 2. Mechanical theory (L. Aschoff) Injuries by the food bolus of the gastric mucosa in the region of the lesser curvature ("gastric path" ) 3. 3. Inflammatory theory (V. Konechny) Gastric origin of ulcers 4. 4. Peptic theory (E. Riegel) 5. 5. Theory of acidosis (P. Balint) 6. 6. Neuro-vegetative theory (G. Bergmann) Hypersecretion and hypermotility of the stomach in persons with constitutional parasympathetic hypertonicity. 7. 7. Immune theory of ulcer. Etiology and pathogenesis

I WOULD. Etiology and pathogenesis 8. 8. Neuro-reflex theory (I. Grekov, N. Strazhesko) Reflex effect on the stomach of other diseases of the abdominal cavity (appendicitis, pancreatitis, cholelithiasis, etc.) 9. 9. Cortico-visceral theory (K. Bykov , I. Kurtsyn) The role of the central nervous system and subcortical centers in dysregulation of the functions of the stomach and 12-pc. 10. Hormonal theory Influence of TSH and ACTH on gastric secretion 11. Dysmotility Duodenostasis and insufficiency of the pyloric sphincter cause reflux and destruction of the mucous membrane by bile acids and lysolecithin. Hypotension of the stomach causes congestion, hypersecretion and gastric ulcer. Hypertonicity causes rapid evacuation, 12-pk acidification and 12-pk ulcer. 12. Infection theory Waste products of H. pylori destroy the mucosal barrier.

I WOULD. Etiology and pathogenesis. Pathogenetic mechanisms Aggression and defense factors Proteolysis Trophic state. Bicarbonate buffer Quantity and quality of mucus Regenerative capacity of the epithelium. Glycosaminoglycans and glycoproteins containing fucose The state of blood supply and innervation. Neurohumoral influences Impaired motor skills Immune disorders. Increased activity of TSH and ACTH Waste products of H. pylory

I WOULD. Clinical picture, course of the disease 1. 1. Pain syndrome Localization in the epigastrium, possible irradiation to the back, hypochondrium, chest Relationship with the nature and time of food intake Seasonal frequency Local (point) pain on palpation in the epigastric region 2. 2. Dyspeptic syndrome Heartburn Belching Nausea Relief vomiting Possible stool problems

I WOULD. Clinical picture, course of the disease 3. 3. Neurasthenic syndrome Irritability Sleep disorder Sweating hypochondria 4. 4. General condition disorder syndrome Fatigue Weakness Loss of appetite Weight loss 5. 5. Syndrome of dysfunction of other organs Pancreas Liver Gallbladder Intestine Cardiovascular system

Gastric phase (no ulcer, symptoms of chronic gastritis) penetrating ulcer. YABAB. . Clinical picture, course of the disease. Phases of the clinical course of peptic ulcer Ulcerative-gastritic phase (unstable mucosal defect, quickly stopping the picture of peptic ulcer) Visceropathic phase (persistent ulcerative defect with a pronounced clinical picture, dysfunction of other organs) Dystrophic phase (physical and mental asthenia, cachexia. Observed with decompensated stenosis ) bleeding ulcer perforation stenosis

I WOULD. Clinical picture, course of the disease. Diagnosis Complaints Hypothesis of the diagnosis Anamnesis Examination Laboratory data Confirmation of the hypothesis Wedge. differential diagnostic radiologist. examination Confirmation of the diagnosis of FGDS with biopsy

X-ray of the stomach Direct projection with an ulcer of the lesser curvature, the arrow indicates the retraction of the greater curvature of the stomach, due to local spasm

Target radiographs of the duodenal bulb Profile, or contour niche on the back wall of the bulb (indicated by an arrow) with an inflammatory shaft in the form of enlightenment

Endoscopic picture of the stomach An ulcer of the anterior wall of the antrum of the stomach: a longitudinal irregularly shaped ulcer covered with white fibrin (indicated by an arrow) is visible; the edges of the ulcer are hyperemic; there is a convergence of mucosal folds to the edges of the ulcer

Targeted radiographs of the duodenal bulb Relief niche, or face niche (indicated by an arrow) with convergence of mucosal folds to it

Endoscopic picture of the stomach An ulcer of the lesser curvature of the stomach (indicated by an arrow) with a tendency to scarring: visible convergence of the mucosal folds to the edges of the ulcer

I WOULD. Clinical picture, course of the disease. Differential diagnosis 1. 1. Diseases of the abdominal organs (liver, gallbladder, pancreas, intestines) 2. 2. Diseases of the esophagus (esophagitis), heart (IHD), lungs (thoracoabdominal syndrome), spine (osteochondrosis) 3. 3. Symptomatic ulcers

Differential diagnostic criteria for peptic ulcer and symptomatic gastroduodenal ulcers. The main criteria for the diagnosis of PU Symptomatic ulcers Age Predominantly young and middle More often elderly and senile Gender More common in men Approximately with the same frequency occurs in men and women symptoms of another (underlying) disease Duration of ulcer history Typically several years No long history of ulcer; often acute onset Presence of preexisting diseases Not typical; only random combinations of peptic ulcer with other diseases can occur. The ulcerative process often develops against the background of another (main) disease (extensive burns, myocardial infarction, pulmonary heart failure, cirrhosis of the liver, hyperparathyroidism, etc.) or diseases for which long-term anti-inflammatory therapy was performed , including steroid drugs (rheumatoid arthritis) and a number of other ulcerogenic drugs (for example, reserpine)

Differential diagnostic criteria for peptic ulcer and symptomatic gastroduodenal ulcers. Seasonality of exacerbations Pronounced Not characteristic Localization of the ulcer More often in the duodenal bulb, less often in the stomach Predominantly in the stomach, less often in the duodenal bulb Number of ulcers In most cases, a single ulcerative defect Often 2-3 or more ulcers, which are often combined with erosions of the mucous membrane Frequency of complications (bleeding, perforation) Up to 15-20% Frequent, can reach 40-70% Average terms of scarring of ulcers with conservative treatment 30-35 days - with the localization of the ulcer in the duodenal bulb, 40-45 days - with the localization of the ulcer in the stomach Terms of scarring ulcers are longer and depend largely on the effectiveness of the treatment of the underlying disease

I WOULD. Treatment. For the convenience of choosing the tactics of treating uncomplicated duodenal ulcers, the following classification was used GASTRITIC phase (no ulcer or remission)) Drug treatment GASTRITIC ULCER phase (open ulcer, no complications)) Drug treatment, laparoscopic vagotomy is possible VISCEROPATHIC phase (Complicated course or unsuccessful drug treatment )) Surgical treatment DYSTROPHIC phase Symptomatic treatment

The main goals of drug treatment of gastric ulcer and duodenal ulcer Relief of pain syndrome Healing of the ulcer Decontamination of the mucous membrane of the stomach and duodenum from H. pylori in order to prevent recurrence

The main goals of rational surgical treatment for gastroduodenal ulcers Mandatory elimination of the pathological substrate (ulcer removal) - the source of complications and antigenic stimulation Correction of the secretory function of the stomach Creation of optimal conditions for adequate evacuation of the contents of the stomach or its stump This does not exclude the eradication of H. pylory

I WOULD. Treatment. Uncomplicated duodenal ulcer Despite the revolution in the therapy of PU, the reported incidence of gastric ulcer and 12 bp does not decrease. The number of patients with perforated ulcer is increasing. The number of patients with bleeding from the upper gastrointestinal tract is increasing, but ulcerative bleeding in this heterogeneous group of patients in terms of etiology is about 50%. At the same time, the number of resections of the stomach with peptic ulcer decreases. 15-20% of patients with duodenal ulcer are operated on for its formidable complications and the same number need planned surgical treatment VI Onopriev, 1995; A. S. Balalykin, 1996; A. G. Khasanov et al. ,

I WOULD. Treatment. Uncomplicated duodenal ulcer According to international statistics, the number of operations for uncomplicated duodenal ulcer has decreased by 75 - 80%. The question is: is such a situation desirable for all patients and is it justified in all cases? The last decade is characterized by an increase in the number of emergency operations for perforated (2 times) and bleeding ulcers (3 times), which resulted in an increase in mortality over this period by 20-25%. But is long-term drug treatment really an equivalent alternative to surgical treatment? Those who have placed and still place too high hopes on conservative treatment will be disappointed by the high rate of relapses and expected complications.

I WOULD. Treatment. Uncomplicated duodenal ulcer overall mortality in peptic ulcer, despite the possibility of drug treatment, remained the same and does not tend to decrease; in surgical clinical observations, the rate of urgent interventions due to complications is growing, the number of emergency operations has increased disproportionately compared to planned ones, which negatively affects the results of operations; The median age of patients with complications of peptic ulcer has increased significantly over the past 20 years.

I WOULD. Treatment. Uncomplicated duodenal ulcer Theoretically, in patients with uncomplicated duodenal ulcer, there are two ways to treat the disease. With such competition, elective surgery must be weighed against the risk factors of medical treatment. - - mortality in the natural course of duodenal ulcer after 5 years was - 1.6% - with drug therapy - 1%, - with early surgical treatment - 0.1%.

I WOULD. Treatment. Uncomplicated duodenal ulcer Fascination with conservative methods of treatment for frequently recurring and long-term ulcers does not cure the disease, but delays the development of its complications V. I. Petrov et al. , 1995; E. M. Blagitko,

I WOULD. Treatment. Uncomplicated duodenal ulcer Operative treatment K Absolute indications include ulcer perforation, profuse gastrointestinal bleeding, decompensated pyloric stenosis, ulcer malignancy. Relative indications are deeply penetrating gastroduodenal ulcers, callous gastric ulcers, gross cicatricial and ulcerative deformities of the stomach and duodenum, accompanied by a violation of the evacuation function of the stomach, as well as repeated gastrointestinal bleeding. Relative indications are visceropathic stage, penetration, multiple ulcers, combined ulcers, recurrence of ulcers after suturing, history of bleeding, age over 50 years.

I WOULD. Treatment. Uncomplicated duodenal ulcer Surgical treatment In addition, surgery is indicated in the following cases: Ulcers resistant to therapeutic methods of treatment (15 - 20%). Negative attitude of some patients to frequently repeated and expensive courses of treatment. The presence of social and ethical problems that make it difficult to conduct appropriate courses of treatment.

I WOULD. Treatment. Surgical treatment In connection with the advent of minimally invasive surgical technologies, indications for surgical treatment are expanding - surgical interventions are possible already in the second gastric ulcer phase

I WOULD. Surgical treatment Arsenal of surgical interventions for ulcerative stenosis Gastroenterostomy, Gastric resection with ulcer removal or "off" , Antrumectomy with vagotomy, Vagotomy with pyloroplasty or gastroduodenoanastomosis, PPV with duodenoplasty.

I WOULD. Treatment. Operative treatment. Classification of resection methods 1. 1. According to the volume of the removed part Subtotal Hemiresections Antral 2. 2. According to the localization of the removed part Distal Median proximal 3. 3. According to the method of completion Gastroduodenal anastomosis (method B-II)) Gastrojejunoanastomosis (method B-IIII)) Gastrojejunoanastomosis on a disconnected loop (according to Ru)

Schematic representation of distal resection of the stomach 1. 1. Billroth-II method 2. 2. Billroth-IIII method modified by Hofmeister-Finsterer 3. 3. Billroth-IIII method modified by Balfour

I WOULD. Treatment. Surgical treatment Currently, the indications for gastric resection have narrowed due to the risk of developing PGRS and relatively high mortality. Resection according to B-II and in the Roux modification was recognized as the most physiological. It is mainly used for stomach ulcers. The indications for economical resections in combination with vagotomy and other organ-preserving operations have been expanded. Their advantages are physiology and minimal lethality. SPV is recognized as the most optimal.

Schematic representation of vagotomy 1. 1. Stem 2. 2. Selective gastric 3. 3. Selective proximal

Scheme of extended selective proximal vagotomy (Kuzin M.I. et al., 1980) Institute of Surgery. AV Vishnevsky RAMS 1. 1. crossed secretory fibers of the vagus nerves along the lesser curvature of the stomach; 2. 2. "crow's foot" of the vagus nerve; 3. 3. skeletal cardia and the lower part (4-5 cm) of the esophagus; 4. 4. denervated greater curvature of the stomach from the antrum to the short arteries of the stomach; 5. 5. anterior and posterior trunk of the vagus nerve.

Schematic representation of pyloroplasty. The dotted line indicates the lines of dissection 3. 3. According to Finney (imposition of anastomosis between the antrum of the stomach and the duodenum)

Schematic representation of pyloroplasty The dotted line indicates the dissection lines 1. 1. According to Heineke-Mikulich (the pyloric part of the stomach and duodenum are dissected along, the resulting hole is sutured in the transverse direction) 2. 2. According to Judd (diamond-shaped excision of the anterior semicircle of the pylorus together with an ulcer)

I WOULD. Treatment. Surgical treatment Pathogenetically substantiated organ-preserving operations can be performed by the laparoscopic method (vagotomy), as well as combined - laparoscopic vagotomy + drainage operation from a mini-access.

A good result of treatment is determined primarily not by the type of surgical intervention, but by the correct choice of it in each case, especially with a duodenal ulcer.

I WOULD. Treatment. Surgical treatment The choice of the method of surgery is determined depending on many factors: 1. 1. Phase of the disease 2. 2. Localization of the ulcer 3. 3. Type of gastric secretion 4. 4. Presence of complications 5. 5. Predisposition to PGRS 6. 6. Patient's condition

I WOULD. Treatment. Surgical treatment When choosing a method of operation, it should be taken into account that vagotomy affects the first phase of gastric secretion, and draining operations affect the second. Stem and selective vagotomy can only be performed in combination with a draining operation (due to pyloric spasm), and PPV can be performed in isolation

Types of gastric secretion Type of secretion Debit hour of hydrochloric acid (mmol) 1 phase 2 phase Normal 1. 1-4. 1 1. 1-5. 9 Asthenic More than 4. 1 5. 9 or less Excitable More than 4. 1 More than 5. 9 Inert 4. 1 or less More than 5. 9 Inhibitory Less than 1.

I WOULD. Treatment. Surgical treatment of PWS has an advantage when it is necessary to act only on the first phase of secretion (asthenic type) With an excitable type of secretion, SV is most often used in combination with antral resection or pyloroplasty. In inert and inhibitory types, gastric resection is indicated, which performs the task of taking the ulcer together with a section of the stomach with impaired trophism Vagotomy and drainage operations give minimal mortality, but the number of relapses reaches 10%

Operations for perforation of the ulcer account for about 30% of all surgical interventions for duodenal ulcer, while mortality ranges from 3 to 12% In 15-20% of gastroduodenal ulcers are complicated by bleeding of the ulcer. Complications. Perforation

I WOULD. Complications. Perforation. Pathogenesis In perforated ulcers, an autoimmune conflict similar to the Arthus phenomenon is recognized as the most reliable cause.

I WOULD. Complications. Perforation. Symptoms and diagnosis Clinical course I. I. The period of "acute abdomen", shock - the easiest to diagnose, the most pleasant to heal. Characteristic symptoms: Main "dagger" pain (90%) Board-like tension of the muscles of the abdominal wall (90%) Ulcerative history (80%) Pneumoperitoneum (85%) (increases to 96% with pneumogastrography) Auxiliary preperforative states Difficulty breathing Anxiety, fear Forced positions Vomiting Hyperleukocytosis Fluid in the abdominal cavity Shchetkin's symptom is not caused

I WOULD. Complications. Perforation. Symptoms and diagnosis II. A period of imaginary well-being Disappear signs of shock Pain intensity decreases The abdomen becomes softer (although tension in the epigastrium is almost always preserved) III. Period of diffuse peritonitis Difficulties in diagnosis are most likely in the second period, as well as with covered and atypical perforations

I WOULD. Complications. Perforation. Differential diagnosis Differential diagnosis is carried out with other acute diseases of the abdominal organs, most often with acute pancreatitis

I WOULD. Complications. Perforation. Differential diagnosis No. Signs Weight values ​​11 Woman 33 22 Age 40 years and older 11 33 Radiation of pain in the lower back 44 44 Error in diet 11 55 No gastritis history 22 66 Repeated attack 33 77 Nutrition increased 22 88 Absence of forced position 33 99 Absence of motor restlessness 11 1010 The abdomen participates in breathing 44 1111 Peristalsis is heard 33 1212 Absence of dullness in the sloping parts of the abdomen 22 1313 Absence of muscle tension in the abdominal wall 44 1414 Hepatic dullness is preserved 33 1515 Shchetkin’s symptom is negative 33 If the sum of the symptom weights is 19 or more, the diagnosis of acute pancreatitis is made

I WOULD. Complications. Perforation. Diagnostic algorithm for perforated gastroduodenal ulcer Perforation of the ulcer? X-ray examination Presence of gas Absence of gas EGDS Presence of an ulcer Absence of an ulcer. Operation Laparoscopy

I WOULD. Complications. Perforation. Treatment of perforated ulcers of the gastroduodenal zone 1. In the presence of indications and conditions (in combination with stenosis, bleeding, penetration, ulcers of the body of the stomach) - economical resection of the stomach + villages. vagotomy. 2. duodenal ulcers against the background of chronic renal failure - economical resection of the stomach + villages. vagotomy, Jabouley or Finney operation + sat down. Vagotomy. 3. Excision of a perforated ulcer (Jadd operation) + sat. vagotomy. Before the development of purulent peritonitis: With purulent peritonitis: 1. Sewing up the perforation, toilet and drainage of the abdominal cavity. 2. Excision of the perforated ulcer and suturing (Judd operation), toilet and drainage of the abdominal cavity. In a serious condition of the patient (stroke, heart attack, etc.) 1. Conservative method of treatment: constant aspiration of gastric contents, intensive antibacterial and detoxification therapy, laparoscopic drainage of the abdominal cavity is possible

Choice of surgical method for perforated gastroduodenal ulcers according to mathematical modeling of long-term results No. Signs Weight values ​​11 Age over 30 years 2828 22 Gastric history 1818 33 Gastric history more than 1 year 2525 44 Ulcer localization in the body of the stomach 3131 55 Ulcerative infiltrate over 1 cm in diameter 4040 66 Hard edges of the ulcer 4848 77 The size of the perforation is more than 0.5 cm 4343 88 Concomitant chronic diseases of the respiratory and cardiovascular systems 2424 If the total weight is less than 73, the prognosis for suturing is favorable

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Peptic ulcer or peptic ulcer is a complex pathological process, which is mainly caused by inflammation of the mucous membrane of the gastroduodenal zone, in most cases of infectious origin, with the formation of local damage to the mucous membrane of the upper parts of the alimentary canal as a response to the endogenous balance of local factors of "aggression" and "protection" .

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The etiological involvement of the alimentary factor is not as significant as it was previously thought, since epidemiological studies have not confirmed the predominant prevalence of PU in those regions where spicy and spicy food is everyday. Smoking causes ischemia and has a direct cytotoxic effect on the mucosa. Gastric secretion directly depends on the functional state of the nervous system, and therefore sedatives are widely used in the treatment of peptic ulcers.

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Technology

A high prevalence of peptic ulcers is observed among people who, due to their professional characteristics, are subjected to psycho-emotional and physical overload in combination with inadequate rest and eating disorders (doctors, telephonists, dispatchers, managers, railway and water transport workers). Among the drugs that contribute to the development of ulcers, one can name NSAIDs (aspirin, indomethacin, etc.) and corticosteroids, antibacterial agents, digoxin, theophylline, reserpine, iron and potassium preparations.

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The hereditary factor is important in 30-40% of patients. In the first degree of kinship, duodenal ulcers occur about 3 times more often than in persons with uncomplicated heredity, and the predisposition to them is more often transmitted through the male line. It has been established that the following signs are genetically determined: an increased number and density of parietal cells per unit surface of the gastric mucosa, an increased content of pepsinogen 1 (increases the risk of an ulcer by 8 times).

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Duodenal ulcers occur 1.5 times more often and are more severe in people with blood type 0 (I) Rh +, with the presence of HLA B5, B15, B35 antigens. The ratio of men and women is 4:1. It is believed that female sex hormones to some extent protect against ulcer formation. After menopause, the ratio of ulcers in men and women levels off. At a young age, duodenal ulcer occurs 13 times more often than gastric ulcer, and in older age groups, gastric ulcer prevails. In recent years, the structure of age-related morbidity has changed and the age range for peptic ulcer disease has expanded due to an increase in the number of "youthful" and "senile" ulcers.

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To date, the leading factors in the formation of ulcerative lesions are hyperproduction of hydrochloric acid and Helicobacter pylori infection. Researchers B. Marshall and D. Warren in 1983 did not suspect that they opened a new era in the study of stomach diseases by opening an incubator after a vacation week and discovering the growth of a culture of spiral bacteria from biopsies of the gastric mucosa obtained from a patient with gastritis. Today we already know that this microorganism causes gastritis in more than half of the world's population, being also the etiological factor in more than 95% of all duodenal ulcers and mails and 90% of benign non-drug gastric ulcers.

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Perhaps N.R. plays a causative role in the occurrence of 60-70% of cases of stomach cancer and other diseases. An obligatory condition for the existence of bacteria H.R. - a certain optimal pH level of 3-6, the presence of urea in the gastric juice and the presence of the gastric epithelium. All strains of H.R. produce a large amount of the enzyme urease, which hydrolyzes the urea of ​​gastric juice, resulting in the formation of carbon dioxide and ammonia. This fact is the basis for the diagnostic methods of N.R. (urea test). Increased production of hydrochloric acid is important in the development of duodenal and gastric ulcers. In most patients with duodenal ulcers, the basal production of hydrochloric acid is approximately three times higher than in healthy people.

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The mechanisms of regulation of the secretion process are diverse. Central stimulation of secretion is initiated by thoughts of food, the sight, smell, and taste of food and begins with the activation of the hypothalamic nuclei of the vagus efferent fibers. Further, the excitation is transmitted through the nerve plexus of the stomach wall to many cells of the mucous membrane. Distension of the stomach with food and stimulation by food components, amino acids, and G-cell proteins of the antrum leads to the release of gastrin. Increasing the level of serum gastrin is a key moment in the endocrine stimulation of acid, because. it activates β-cells located around the parietal cells in the lower third of the gastric glands and rich in histamine.

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Gastrin binds to the surface receptors of ECL cells, as a result of which the release of histamine is stimulated, which, in turn, binds to the H2 receptor and starts the entire intracellular biochemical chain, the result of which is the release of hydrochloric acid into the lumen of the glands and stomach. At the end of the gastric phase of secretion, when the pH in the antrum reaches a value below 3, reverse processes of inhibition of gastric secretion begin. This is due, first of all, to the release of antral somatostatin from D-cells, which inhibits not only the function of G-cells of the antrum and the production of gastrin by the “feedback” type, but also being a “universal brake fluid” for other hormones and biologically active substances.

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In the intestinal phase of secretion, when gastric contents with a pH below 4 enter the duodenum, secretin is released from the cells of the intestinal mucosa, which inhibits both gastric secretion and gastrin release. Prostaglandins, which act on the parietal cell through a special receptor, also have an inhibitory effect on gastric secretion.

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But along with aggressive factors (hyperproduction of hydrochloric acid and pepsin, H. pylori bacteria, traumatization of the gastroduodenal mucosa, impaired evacuation-motor function of the stomach and duodeno-gastric reflux, drugs with an ulcerogenic effect), there are also protective factors. These are the surface epithelium and the mucous-bicarbonate barrier covering it, active cellular regeneration, sufficient blood flow in the mucous membrane, cytoprotective substances.

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It is traditionally believed that in the pathogenesis of pyloroduodenal ulcers, the increase in aggressive factors is more important, and in case of mediogastric ulcers, the weakening or failure of protective factors is more important. That is why in the treatment of gastroduodenal ulcers, many medicines are used with a variety of application points.

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Localization of peptic ulcer: gastric ulcer duodenal ulcer (bulbs, postbulbar) combined gastric and duodenal ulcers gastrojejunal ulcer.

Classification of PU (according to V.G. Perederiy).

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With an ulcer of the cardiac section or the posterior wall of the stomach, the pain is localized behind the sternum and radiates to the left shoulder, resembling angina pectoris. Pain with an ulcer of the pyloroduodenal zone radiates to the back, right hypochondrium, under the right shoulder blade. Pain with an ulcer of the body of the stomach is localized in the epigastric region on the left near the xiphoid process and does not radiate anywhere.

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Characteristic is the rhythm of pain and the connection with the use of food. With the localization of the ulcer in the cardiac region or on the back wall of the stomach, the pain appears immediately after eating. An antral (prepyloric) stomach ulcer is indicated by hunger pain that occurs 2-3 hours after eating or late at night. The pain lasts until the stomach is emptied.

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The main symptom is pain in the epigastric region 1.5-3 hours after eating. This is a hungry, nocturnal pain that goes away after eating or alkalis. In patients with concomitant duodenitis, persistent night pains are observed. Sometimes the pain is not related to food. The seasonality of pain with periods and exacerbations in autumn and spring is very characteristic.

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In addition to pain, patients are concerned about nausea and vomiting, which occurs at the height of pain and, as a rule, brings relief. Heartburn is a burning sensation in the region of the lower third of the sternum, it can be the equivalent of pain, it can be aggravated by changing the position of the body, bending down. The occurrence of heartburn is due to reflux, i.e. the reverse flow of the contents of the stomach into the esophagus due to a decrease in the tone of the cardiac closure and an increase in intragastric pressure. In addition to reflux, esophagitis is also important in the development of heartburn. In addition, there may be sour belching, bloating, and persistent constipation with sheep's stools.

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A physical examination reveals: autonomic dysfunction syndrome (excessive sweating, red and white dermographism, sleep disorders, increased irritability), local soreness and muscle tension in the epigastric region and the pyloroduodenal zone, increased gastric motility and spastic condition of the colon.

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Verifies the ulcer endoscopically - gastrofibroduodenoscopy. Each endoscopy should be accompanied by a biopsy to solve 3 tasks: conducting a CLO test for the express diagnosis of Helicobacter pylori infection, taking biopsy material for subsequent seeding on selective media, obtaining a culture of H.R. and determining its sensitivity to various antibacterial drugs, conducting a histological examination of biopsy material to exclude rare causes of duodenal ulcers and clarify the severity of chronic gastritis.

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Breath test with urea. Currently the most sensitive and easy to implement. The method is based on the fact that after oral administration of urea solution labeled with 13C or 14C, urease H.R. metabolizes labeled urea and releases labeled carbon dioxide, which is determined in the exhaled air for 10-30 minutes. In contrast to serological reactions, the test is positive for current H.R. infection. .

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Gatekeeper's ulcer. It is characterized by an atypical clinical syndrome, bouts of nausea, rapid weight loss, pain loses its frequency, is permanent, aching intensifies immediately after eating. Bleeding is characteristic (sometimes this is the first sign of the disease). Indicators of gastric secretion remain normal, d-z is confirmed radiologically and endoscopically by ulcerative defects along the lesser curvature, more often on the posterior wall of the pylorus.

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Giant ulcers. More often detected in the elderly, have dimensions of at least 3 cm in diameter. They are located on the lesser or greater curvature of the stomach, in the bulb of the duodenum 12. They are characterized by an atypical clinical picture - the pain may resemble renal colic or pancreatitis. Giant ulcers are asymptomatic for a long time and are manifested by bleeding or penetration.

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PU should be differentiated from symptomatic ulcers, Mallory-Weiss syndrome, Zollinger-Ellison syndrome. Acute ulceration of the mucous membrane of the stomach and duodenum includes stress, aspirin-induced, glucocorticoid-induced, heparin, non-steroidal anti-inflammatory drugs. They can occur with acute coronary syndrome, liver cirrhosis, chronic renal failure, thyroid diseases, burns (Carling ulcers), alcohol and other toxicant abuse, etc.

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They are localized more often in the area of ​​the bottom and body of the stomach. Patients have pain in the epigastric region, heartburn, nausea, belching, dry mouth, general weakness, tachycardia. D-ka FGDS, Treatment - the abolition of ulcerogenic drugs, the appointment of H2 histamine blockers or a proton pump blocker, sucralfate.

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Mallory-Weiss syndrome - cracks-ruptures of the mucous membrane of the cardial part of the stomach, the direct cause of them is repeated vomiting. Spasms of the lower esophageal closure. Cracks-ruptures are localized along the longitudinal axis of the stomach, occasionally capture the submucosal and muscular layers. The clinic is bloody vomiting. Treatment - stopping bleeding, prescribing proton pump blockers.

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Mallory-Weiss syndrome Cracks are ruptures of the mucosa of the cardial part of the stomach, the direct cause of them is repeated vomiting. Spasms of the lower esophageal closure. Cracks-ruptures are localized along the longitudinal axis of the stomach, occasionally capture the submucosal and muscular layers. The clinic is bloody vomiting. Treatment - stopping bleeding, prescribing proton pump blockers.

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Zollinger-Ellison syndrome. Ulcerogenic gastrinoma (gastric-secreting neuroendocrine tumor), clinically manifested by recurrent duodenal ulceration, diarrhea (inactivation of pancreatic lipase). Acid-forming function - panhyperchlorhydria. The concentration of gastrin in the blood is increased. Treatment is proton pump inhibitors.

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Therapeutic nutrition Diets No. 1a and 1b are prescribed in the acute phase for 2-3 days, after which they are transferred to diet No. 1, which stimulates the processes of reparation of the mucous membrane, prevents the development of constipation, and restores appetite. The goal is mechanical, thermal and chemical sparing of the mucosa. Food is given boiled, but not pureed, 5-6 times a day. The diet includes white stale bread, soups from cereals, vegetables, well-boiled cereals, mashed potatoes, poultry meat. There is an opinion that the appointment of tables 1, 1a and 1b is suitable only for persons with a complicated ulcer.

"Peptic ulcer of the stomach and duodenum" - Established etiological factor. The stomach ulcer heals. Therapeutic mode. Serological method. Hydrochloric acid overproduction and infection. 1 week therapy. Peptic ulcer or peptic ulcer. Localization of peptic ulcer. Carrying out gastrofibroduodenoscopy. Breath test with urea. High infection eradication rates.

"Gastritis" - Natural gastric juice (HCl) and atsedin-pepsin. Classification of gastritis. The mucous membrane of the stomach in chronic gastritis. About half a ton of various food passes through the stomach. Difficultly coordinated movements. Treatment. Chronic gastritis. The stomach is a hollow sac with a volume of only 80 ml. bacterium Helibacter pylori.

"Dyspepsia" - Infectious factors. Prevention. Dispensary observation of children. Diagnostics. selective blockers. Autoimmune gastritis. Histological studies. Esophagogastroduodenoscopy. protective layer. functional dyspepsia. Clinic. Pathogenesis. Antacids. Toxic-infectious form. nutritional factors.

"Acute appendicitis" - The contents of the stomach. Search for the phenomenon of pain migration. Acute appendicitis. Frequent diagnosis. Recovery. Appendix. The correctness of the proposed diagnosis. "resorption" of the infiltrate. Destructive appendicitis. Appendicitis. Tampons drained the right iliac fossa and small pelvis. Removal of the diverticulum.

"Prevention of diseases of the digestive system" - Stress. Risk factors. Disposable. To give up smoking. Fatal. Wrong nutrition. The most common diseases of the digestive system. Low physical activity. Proper nutrition. Prevention. Prevention of diseases of the digestive system. Personal hygiene. Diseases of the digestive system.

"Acute pancreatitis" - Treatment of patients with persistent pancreatic necrosis. The possibility of using minimally invasive surgical aids. Distribution of patients by sex and age. Easy degree. PON frequency. Severe acute pancreatitis. Distribution of patients with OP according to the etiological factor. The frequency of forms of pancreatic necrosis. widespread necrosis.

There are 18 presentations in total in the topic

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Peptic ulcer of the stomach and duodenum (PU) is a chronic disease of the gastrointestinal tract, the main manifestation of which is the formation of a fairly persistent ulcer in the stomach and/or duodenum (DU). In the International Classification of Diseases (ICD-10), PU corresponds to the name peptic ulcer disease. PU is a chronic and recurrent disease that is prone to progression and involvement in the pathological process, except for the stomach, other digestive organs and the whole body. Inadequate treatment of PU leads to complications that threaten the life of the patient.

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Slide 5: Etiology and pathogenesis

the presence of the microbe Helicobacter pylori on the gastric mucosa; decrease in mucosal resistance to gastric acid; increased production of stomach acid (for example, the effect of caffeine); smoking; regular use of non-steroidal anti-inflammatory drugs, such as, for example, aspirin, ibuprofen, diclofenac and naproxen (Emox, Nalgesin) and glucocorticoid hormones (prednisolone, etc.), which directly damage the mucosa; stress.

Slide 6: Genetic factors that contribute to the occurrence of ulcers:

high level of maximum secretion of hydrochloric acid; increase in the number of parietal cells and their increased sensitivity to gastrin; trypsin inhibitor deficiency; fucomucoprotein deficiency; increased content of pepsinogen in blood serum and urine; excessive production of gastrin in response to stimulation; gastroduodenal dysmotility - prolonged food retention in the stomach; increased formation of pepsinogen; insufficient production of secretory Ig A and prostaglandins; serological blood markers: reduce the resistance of the gastric mucosa, blood type 0 (1), positive Rh factor; hereditary markers of histocompatibility for duodenal ulcer - HLA B5 (in the Ukrainian population - B15, in the Russian - B14); congenital deficiency of antitrypsin; lack of excretion of factors of the ABO system with gastric juice (the risk of PU increases by 2.5 times).

Slide 7: Classification according to Mazurin A.V. et al. (1984), with additions on the etiological factor

1. Clinical and endoscopic stage: acute ulcer; the beginning of epithelialization; healing of an ulcerative defect of the mucous membrane with existing gastroduodenitis; clinical and endoscopic remission. 2. Phases: exacerbation; incomplete clinical remission; clinical remission. 3. Localization: stomach; duodenum (bulb; bulbous department); double localization. 4. Form: no complications; with complications (bleeding, penetration, perforation, pylorus stenosis, perivisceritis). 5. Functional characteristics: acidity of gastric contents and motility (increased, decreased, normal). 6. Etiological characteristics: Helicobacter pylori associated; Helicobacter pylori unassociated.

Slide 8: Clinical manifestations of PUD

There are also asymptomatic ulcers, but this is not a traditional situation (ulcers resulting from medication often occur without complaints). The most common symptoms are: 1. dull aching or burning pain in the abdomen, primarily in the central region of the upper abdomen. Gastric ulcers are more likely to hurt during meals, while duodenal ulcers - a couple of hours after eating or on an empty stomach, and eating rather relieves symptoms; 2. nausea and/or vomiting; 3. pain that is relieved by eating or taking medicines that lower the acidity of the stomach contents (antacids); 4. pain that gets worse a couple of hours after eating or sometimes also before eating; 5. pain that wakes you up at night; 6. weight loss, lack of appetite. If the ulcer bleeds, you may have; 7. vomiting, in the vomit there may be bright red blood or brown blood resembling coffee grounds; 8. black feces.

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Slide 10: Clinical manifestations of complicated PU

Complicated course of PU is observed in 10-15% of cases, twice as often in boys. Bleeding is the most common complication of PU (80% of complications). Clinical signs of acute bleeding in PU: vomiting of "coffee grounds", vascular collapse and signs of anemia of the body - pallor, general weakness. Often, against the background of the development of bleeding, a weakening of the pain syndrome is observed, which can lull the doctor's vigilance. Perforation. (7-8%); Ulcer perforation usually begins with an attack of acute "dagger pain", which is accompanied by a clinic of an acute abdomen, tension in the epigastric region, abdominal wall, and symptoms of peritoneal irritation. Note the weakening or absence of peristalsis. These clinics are confirmed by x-ray examination - the presence of free gas under the liver during x-ray examination of the abdominal organs. Penetration. (1-1.5%). Duodenal ulcers penetrate into the head of the pancreas, liver, bile ducts, hepatoduodenal ligament. Gastric ulcers penetrate into the lesser omentum and body of the pancreas. The main clinical manifestations are sharp pains that radiate to the back, vomiting that does not bring relief, heartburn bothers. Penetration is characterized by constant pain, loss of a clear connection with food intake. A characteristic radiological symptom of penetration is an additional shadow of a contrast agent next to the examined organ. Deformity and pyloroduodenal stenosis. (10-12%). Patients feel the overflow of the stomach, nausea, belching. In severe cases, vomiting of stagnant stomach contents is observed. The patient can provoke vomiting himself to get a feeling of relief. The patient is losing weight. In typical cases, there is peristalsis of the hourglass type, the phenomenon of splashing on palpation in the epigastric zone.

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Slide 12: Paraclinical examination methods for PU

1. Laboratory research. 1.1 Mandatory (at the present stage of development of gastroenterology): Complete clinical blood count. General clinical analysis of urine. Analysis of feces for eggs of worms. Coprocytogram. Total protein to blood protein fractions. Histological (cytological) examination during endoscopy. HP tests: rapid urease, bacteriological, respiratory urease test, serological (IFA), IFAS analysis of HP antigen concentration in feces, polymerase chain reaction (PCR). Intragastric pH-metry. 1.2. According to the indications: Analysis of feces for occult blood (Gregersen's reaction). A blood test for hormone levels to detect hypergastrinemia, hypersomatotropinemia. Immunogram.

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2. Instrumental studies and diagnostic criteria: Study of gastric secretion: Intragastric pH-metry. Fractional study of gastric juice (detection of hyperacidity, increased proteolytic activity). Fibroesophagogastroduodenoscopy (FGDS) with targeted biopsy, diagnosis of HP infection is carried out for the purpose of diagnosis and 3-4 weeks after the start of treatment with complete epithelialization of the ulcer.

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Slide 14: Endoscopic criteria for the stages of PU

1. Phase of exacerbation. a) Stage I - acute ulcer. Against the background of pronounced inflammatory changes in the gastric mucosa and duodenum - a defect (defects) of a rounded shape, surrounded by an inflammatory shaft; pronounced edema. The bottom of the ulcer with a layer of fibrin. b) Stage II - the beginning of epithelialization. The hyperemia decreases, the inflammatory shaft is smoothed out, the edges of the defect become uneven, the bottom of the ulcer begins to clear from fibrin, and convergence of the folds to the ulcer is outlined. 2. Phase of incomplete remission. c) stage III - healing of the ulcer. At the site of repair - the remains of granulations, red scars of various shapes, with or without deformation. Signs of gastroduodenitis activity persist.

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3. Remission Complete epithelialization of the ulcer (or "calm" scar), there are no signs of concomitant gastroduodenitis. When conducting a targeted biopsy, an express diagnosis of HP is performed; histological and microbiological diagnosis of HP; histological (cytological) verification of the diagnosis, differential diagnosis with acute ulcers is carried out. X-ray examination is currently of an auxiliary nature. It is used mainly for the diagnosis of motor-evacuation disorders, duodenostasis, cicatricial and ulcerative deformities of the stomach and duodenum. For diagnostic purposes with absolute contraindications to endoscopy. Radiological criteria for ulcers: "niche" symptom, convergence of folds, etc. are rare in children.

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Ultrasound examination of the abdominal organs The examination is carried out once for screening the diagnosis of concomitant pathology.

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Slide 17: Treatment of PUD

The volume of therapeutic measures depends on the localization of the ulcer (stomach or duodenum), the phase of the disease, the severity of the course, the presence of complications, the relationship with HP, the leading pathogenetic mechanisms and the clinical and endoscopic symptom complex. According to the tradition that has developed in domestic pediatrics, the treatment of a patient with a newly diagnosed ulcer and with its exacerbation is carried out in a hospital. At the same time, many foreign pediatricians are more reserved about recommending inpatient treatment. During an exacerbation, the average duration of inpatient treatment is about 1 month. 1. Mode. In the first weeks of hospital stay, bed or semi-bed rest. 2. Nutrition. Diet tables No. 1a, 1b, and then N5 are assigned sequentially. Given the low caloric content of the N1 diet options, the choice of motor regimen depends on the duration of its administration. At the heart of the diet therapy of PU is the principle of preventing thermal, chemical and mechanical irritating effects on the ulcer. That is, very hot or cold food, extractive, spicy, dishes, coarse food rich in dietary fiber are excluded. When PU is complicated by bleeding, the Meilengracht diet is prescribed, which includes puree enriched with proteins, salts and vitamins. In case of HP-associated peptic ulcer in Ukraine, the following treatment regimens are officially recommended, which are based on the provisions of Maachstricht Consensus 2000. In the treatment of HP-associated forms of gastritis and PU in children, combined first and second line therapy is consistently used.

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Slide 18: The main drugs that are used to eradicate HP

1. Bismuth preparations. Denol in a single dose of 4 mg per 1 kg of weight twice a day, or 120 mg 2 times a day (up to 7 years), 240 mg 2 times a day (after 7 years). An analogue of Denol is the Ukrainian drug Gastro-norm 2. Antibiotics: Amoxicillin (flemoxin-solutab) in a single dose of 25 mg per 1 kg of weight (the maximum dose should not exceed 1.0 g); For children up to 7 years 500 mg 2 times a day, after 7 years 1000 mg 2 times a day. Clarithromycin (erythromycin) at a dose of 7.5 mg per 1 kg of body weight per day in 2 doses (the maximum daily dose should not exceed 500 mg). Roxithromycin 5-8 mg per 1 kg of weight per day in 2 doses (maximum dose - up to 300 mg). 3. Nitroimidazole: metronidazole 250 (up to 7 years) 500 mg (after 7 years) 2 times a day or 20-40 mg per 1 kg of weight. 4. Nitrofurans: furazolidone 0.05-0.1 g 4 times a day, up to 20 mg per 1 kg of weight per day. 5. Histamine H2 receptor blockers: famotidine 20-40 mg per day or ranitidine. 6. Proton pump inhibitors: omeprazole in a single dose of 0.5 mg per kg of weight 1-2 times a day.

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Slide 19: Schemes of rational anti-Helicobacter peptic ulcer therapy in children

Three-component first-line therapy options for children (treatment duration 7 days). I. Bismuth based schemes. 1. Dn+Fl+Me. 2. Dn+Fl+Fur. 3. Dn+Fl+Cl. 4. Dn+Fl+Er. II. Schemes based on histamine H2 receptor blockers. 1. Fa + (Ra) + Fl + Fur. 2. Fa+Fl+Me.

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III. Schemes based on proton pump inhibitors. 1. Ohm+Fl+C. 2. Ohm+Cl+Fur. IV. Second line quadruple therapy options for children (treatment duration 7 days). 1. Dn+Fa+Fl+Fur. 2. Dn+Fa+Cl+Fur. 3. Dn+Fa+Fl+Me. 4. Dn+Fa+Fl+Me. 5. Dn+Ohm+Fl+Fur. 6. Dn+Ohm+Cl+Fur. 7. Dn+Ohm+Fl+Me. 8. Dn+Ohm+Cl+Me. List of abbreviations for drug names: Dn - Denol Er - erythromycin. Cl - clarithromycin. Om - ompeprazole. Ra - ranitidine. Fa - famotidine. Fl - flemoxin - solyutab.

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Care: 1. carefully follow the treatment prescribed by your doctor; 2. regularly come to follow-up control; 3. do not smoke; 4. if you have had a stomach or duodenal ulcer, or if you have the symptoms described above, then: avoid medicines that irritate the stomach, such as aspirin, ibuprofen, diclofenac and naproxen. Take paracetamol instead; 5. eat healthy. Several small meals a day are better than 2-3 large meals. Follow the diet prescribed by your doctor; 6. Avoid coffee, including decaffeinated coffee, alcohol, cola drinks, and all foods and drinks that can irritate the stomach. 7. get enough rest and sleep; 8. Be physically active and follow your doctor's advice. If complaints persist or worsen, consult your doctor

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