1. At what age is duodenal ulcer most often diagnosed? Duodenal ulcer often develops at the age of 20-60 years, and the peak falls on the fourth decade of life. The lifetime risk of developing a duodenal ulcer is about 1:14 for both sexes. 2. What causes a duodenal ulcer? Helicobacter pylori, a gram-negative microorganism, often accompanies peptic ulcers. Ulcers can occur with increased acid secretion, normal secretion, or after operations aimed at reducing secretion, such as vagotomy. Recurrent ulcers or multiple ulcerations may indicate endocrine disease. It is believed that the violation of the protective barrier of the duodenal mucosa also contributes to ulcerogenesis. 3. Is an increase in acid secretion a prerequisite for the development of peptic ulcers? No. Increased secretion of acid and pepsin in the stomach plays an important role in the formation of ulcers, but it is noted in only 40% of patients with ulcers. 4. Name the clinically important complications of H. pylori infection. a) Peptic ulcer. H. pylon is found in more than 90% of peptic ulcers. This microorganism is present in almost half of the population, but only a small number develop peptic ulcers. H. pylori can be part of the normal human gastric flora; antigens to the microorganism were found in South American mummies up to 1700 years old. b) Stomach cancer. A close relationship was noted between stomach cancer and H. pylori, which is now considered a Group I carcinogen. The microorganism can also cause the formation of lymphoma from the lymphoid tissue of the mucous membrane. c) Barrett’s disease is possibly associated with H. pylori as well as gastroesophageal reflux. H. pylori is likely to exacerbate gastropathy and ulcers associated with nonsteroidal anti-inflammatory drugs (NSAIDs). 5. What is the most commonly used test to detect H. pylori? The CLO test (a method for determining urease activity) is most often used to detect H. pylori. H. pylori secretes urease, which breaks down urea into ammonia and bicarbonate, increasing the pH. The CLO test can be performed during endoscopy by taking a scraping of the mucous membrane of the antrum. If endoscopic examination is not feasible, an enzyme-linked immunosorbent assay can be performed to detect anti-I. pylori antibody titers (IgA and IgG). Bacteriological testing is used if it is necessary to resist bacterial resistance to antibiotics. 6. What other risk factors are there for developing duodenal ulcers? a) The main risk factor is cigarette smoking; avoiding it is a key component of ulcer treatment. b) Duodenal ulcer often develops in patients with the first (0) blood group, as well as in the presence of leukocyte antigens HLA-B5, B12 and BW35. c) NSAIDs contribute to the formation of ulcers by suppressing the systemic production of prostaglandins. d) Chronic pancreatitis, cirrhosis, emphysema and alpha-1 antitrypsin deficiency. 7. What endocrine disorder is accompanied by severe peptic ulcer disease? 50-85% of patients with multiple endocrine neoplasia (MEN type I) have gastrinoma with severe ulcerative diathesis. 8. What other endocrine disorders should be excluded? If a patient with MEN type I, then a pituitary tumor and hyperparathyroidism should be suspected. 9. How is peptic ulcer clinically manifested? a) Pain in the epigastrium, irradiation to the back may indicate the involvement of the pancreas; can often be removed with food or antacids. Nausea and vomiting are possible. b) Bleeding from the upper gastrointestinal tract. c) Obstruction of the outlet of the stomach due to spasm of the pylorus, the formation of an inflammatory infiltrate, scarring or fibrosis of the duodenum. d) Perforation. Requires emergency surgery and leads to death in 5-10%. In the history of a patient with perforation, there may be no signs of peptic ulcer, especially if the ulcer is located on the anterior wall of the duodenum. 10. How does the location of the ulcer affect its clinical manifestations? With ulcers of the anterior wall (usually the initial part of the duodenum), perforation may occur with the development of peritonitis with free gas in the abdomen. With posterior ulcers, arrosion of the gastro-duodenal artery or pancreas is possible. 11. Between what diseases are differential diagnostics performed for epigastric pain? In addition to peptic ulcers, epigastric pain can be caused by gastroesophageal reflux, gastritis, stomach cancer, biliary tract disease, pancreatitis or pancreatic cancer, and myocardial ischemia. 12. What research should be done for epigastric pain? When? Patients with recurrent upper abdominal pain should be evaluated. Fibroesophagogastroduodenosconia (EGDS) is preferred, although upper GI contrast x-rays can be performed. During the EGDS, the CLO test can be performed according to the indications. Ultrasound is performed if gallbladder disease is suspected, and baseline electrocardiogram should be obtained if in doubt about coronary artery disease. 13. How is duodenal ulcer treated? – Diet: you should stop taking aspirin and NSAIDs. Alcohol, caffeine and especially nicotine should be avoided (do not smoke, do not chew). – Antacids: Neutralizing gastric acid may provide symptomatic relief, but its effect on ulcer healing is not fully understood. – Antagonists of H2-receptors: cimetidine and rapitidine reduce acid secretion in the stomach due to the blockade of H2-histamine receptors. – Sucralfate: This drug adheres to the base of the ulcer, creating a protective cover. Cannot be used concurrently with drugs that reduce acid secretion, since an acidic environment is required to activate sucralfate. – Proton pump inhibitors: omeprazole blocks the hydrogen-potassium adenositriphosphatase pump in the parietal cells of the stomach, reducing the release of hydrogen ions. It is usually reserved for cases where first-line therapy (eg H2 receptor antagonists) fails. – Destroy H. pylori: if H. pylori is detected, then therapy with a combination of three drugs (bismuth, tetracycline and metronidazole) in combination with an H2-receptor antagonist in 90% can achieve a cure. If such treatment is ineffective, then erythromycin, amoxicillin-omenrazole or erythromycin-omeprazole can be added to the regimen. 14. What is the likelihood of relapse after drug therapy? Approximately 75-95% of duodenal ulcers heal in 4-6 weeks. The probability of relapse within 1 year after drug therapy is 70%, so repeated courses of treatment are necessary. 15. What complications are possible with drug therapy? H2 receptor antagonists can cause mental disorders and gynecomastia. Cimetidine, in particular, can affect the metabolism in the liver of warfarin, phenytoin, theophylline, propranolol and digoxin, which leads to an increase in their concentration in serum. Omeprazole can cause hypergastripemia by blocking acid secretion in the stomach. The development of resistance of H. pylori to antibiotics, especially to metronidazole, is possible, therefore it is recommended to start treatment with a combination of three drugs, including at least two antimicrobial drugs and an acid secretion inhibitor. 16. What is the difference between the examination for recurrent or multiple ulcers? To the previously mentioned methods should be added the determination of the level of gastrin in serum; consider the possibility of an endocrine disorder. Stop taking omeprazole before testing. In Zollinger-Ellison syndrome, gastrin secretion by a tumor from the islet cells of the pancreas leads to multiple or refractory ulcers (normal serum gastrin levels <200 pg / ml; in Zollinger-Ellison syndrome, it is usually> 500 pg / ml). 17. What if the gastrin level is borderline (200-500 pg / ml)? A secretin stimulation test can be used to diagnose Zollinger-Ellison syndrome. Intravenous jet injection of secretin (2 U / kg) should lead to a rise in gastrin levels by 150 pg / ml within 15 minutes. 18. What are the indications for surgical treatment of duodenal ulcers? Indications for surgery: failure to stop bleeding with conservative treatment (> 6 doses of red blood cells transferred in 24 hours), obstruction; lack of effect from drug terapin. Ulcer perforation is usually treated surgically, except when peritonitis has not developed 24 hours after perforation and an upper GI X-ray with gastrografin confirms that the perforation is reliably covered. 19. What operations are used to treat duodenal ulcers? a) Stem vagotomy with pyloroplasty or gastroeyuposgomy. b) Stem vagotomy and aptrumectomy with Billroth I or Billroth II anastomosis. c) Subtotalp resection with anastomosis but Billroth I or Billroth II. d) Highly selective vagotomy. e) Gastrectomy. 20. How is Billroth I or Billroth II anastomosis applied? The Billroth I operation is an anastomosis of the gastric stump with the duodenum (gastroduodenostomy). Anastomosis according to Billroth II is formed by suturing the loop of the jejunum to the stump of the stomach (gastrojejunostomy). Both methods are acceptable. 21. Which method is better, Billroth I or Billroth II? The advantages of the Billroth I method is that it does not form a duodenal stump and only one line of sutures is formed, and not two (as with the Billroth II method). The failure of the duodenal stump is an emergency and requires immediate laparotomy. Billroth II surgery can also complicate the adductor loop syndrome. Gastritis due to bile flow can develop in any way. Anastomosis but Billroth I is more physiological – proteins and fats are better digested. The disadvantage of the Billroth I method is that with it more often obstruction of the outlet part of the stomach occurs due to the recurrence of an ulcer or tumor, therefore, as a rule, it is not recommended to form an anastomosis according to Billroth I in gastric cancer. 22. What is the adductor loop syndrome? Pain in the abdomen after eating, which often disappears after vomiting (vomit mixed with bile). Narrowing of the zone of the gastro-duodenal anastomosis according to Billroth II leads to the accumulation of bile and pancreatic juice in the adductor loop of the small intestine. The pain disappears when this fluid passes into the stomach, which can lead to vomiting with an admixture of bile and severe reflux gastritis. 23. How to prevent adductor loop syndrome? To do this, during the operation, a short and non-twisted adductor loop and a narrow Billroth II anastomosis are formed. Billroth I anastomosis prevents the development of the syndrome. 24. What is the likelihood of ulcer recurrence after surgical treatment? – Vagotomy and hpyloroplasty: 10% – Vagotomy and antrumectomy: 2-3% – Highly selective vagotomy: 10-15% – Subtotal resection: 1-2% – Gastrectomy: <1% 25. What is the mortality rate for these operations? – Vagotomy and pyloroplasty: 1% – Vagotomy and antrumectomy: 1-3% – Highly selective vagotomy: 0.1% – Subtotal resection: 1-2% – Gastrectomy: 2-5% 26. How will you treat duodenal ulcer perforation? First, resuscitation is carried out (to ensure the patient’s airway, breathing and hemodynamics). Place a nasogastric tube, rinse the stomach. Graham’s operation is widespread – closing the hole with a strand of the stuffing box. In patients with stable hemodynamics, suturing of the ulcer with highly selective vagotomy can be added. An alternative surgical treatment for patients with recurrent peptic ulcers or with refractory peptic ulcers is vagotomy with antrumectomy. 27. What are the long-term results after Graham closure of ulcer perforation? In a third of patients, symptoms of the disease do not occur, in a third, the symptoms are amenable to drug treatment, and a third requires another operation for the ulcer. 28. Who is Billroth? Austrian surgeon Christian Albert Theodor Billroth (1829-1894) is known for being the first to perform gastric resection (1881) and to make changes in the technique of forming intestinal anastomoses. American surgeon William Halstead studied with him during his internship in Vienna. 29. What complications are possible after operations for duodenal ulcers? a) The failure of the duodenal stump can occur within the first week after antral resection and Billroth anastomosis. Treatment consists in immediate reoperation (drainage and suturing of the stump). Additionally, complete parenteral nutrition may be required. b) Violation of gastric evacuation may result from anastomotic edema or gastric atony due to vagotomy. This complication usually resolves on its own within 3-4 weeks. c) The source of bleeding may be a suture line, an unnoticed ulcer or other pathology of the gastric mucosa. Bleeding after gastrectomy often stops spontaneously, but endoscopic intervention is sometimes required. 30. Where can ulcers recur after surgery? Ulcers usually form in the wall of the intestine (jejunum, duodenum) near the anastomosis. 31. Why do ulcers recur? The cause may be inadequate resection of the stomach, incomplete vagotomy, inadequate drainage of the gastric stump (retention of gastric contents proximal to the anastomosis), or preserved antrum (with Billroth II anastomosis). 32. How does gastritis relapse develop? Reflux of bile or pancreatic juice into the stomach during anastomosis according to Billroth II can cause significant irritation of its mucous membrane, manifested by chronic pain after eating. For persistent pain, an endoscopic examination should be performed to assess the mucosa and surgical reconstruction should be considered, usually with a Roux-en-Y gastrojejupoanastomosis (with a 40 cm long jejunal abduction loop). 33. What is dumping syndrome? With stem vagotomy, the innervation of the stomach and the pylorus is disrupted, which leads to an uncontrolled rapid release of hyperosmolar gastric contents into the proximal small intestine. Sudden changes in osmotic pressure and glucose concentration can be manifested by palpitations, sweating, flushing, weakness, nausea, abdominal cramps, and fainting. Eating small amounts of dry foods that are low in carbohydrates can help relieve the condition. Anticholinergics also help. Dumping syndrome is observed in the early postoperative period in 10-20% of patients, but in 1-3% it becomes chronic. 34. How is pyloric stenosis treated? The first step is to replace fluid loss and perform decompression with a nasogastric tube. Prolonged vomiting can lead to metabolic alkalosis (loss of hydrogen ions), which must be corrected by infusion of saline. Surgical treatment should consist of vagotomy with gastrojejunostomy, or resection of the stenotic site with anastomosis but Billroth II, or resection of the stomach.