1. TASHKENT - 2011 1

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3. Erect radiographic image of esophagus (lower portion), stomach and first part of duodenum after ingestion of contrast medium 3

4. Topography and internal surface of a stomach (blue line represent notional lines marking the parts of the stomach) 4

5. Microscopic section of a gastric gland 5

6.  THE PARIETAL CELLS – acid secretion  THE CHIEF CELLS – pepsinogen secretion  THE ENDOCRINE CELLS: ◦ The G-cells – gastrin secretion ◦ The D-cells – somatostatin secretion ◦ The ECL-cells – histamine production  THE MUCOUS NECK CELLS – mucus secretion 6

7. Components involved in providing gastroduodenal mucosal defense and repair 7

8. Primary chronic recurrent disease of upper gastrointestinal tract associated with circumscribed ulcers within stomach and duodenum 8

9. is disruption of the mucosal integrity of the stomach and/or duodenum leading to a local defect or excavation due to active inflammation 9

10. 1 – submucosa 2 – hard, undermined margin 10

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12.  A break in the mucosa not penetrating muscularis mucosa  Peristalsis is not affected  Heals rapidly 12

13.  Duodenal ulcers (5x) > gastric ulcers  ♂ (4x) > ♀  Urban resident > rural resident 13

14.  Helicobacter pylori  NSAIDs (aspirin) 14

15.  Healthy subjects 20-50%  Chronic active gastritis 100%  Duodenal ulcer >90%  Gastric ulcer 50 - 80%  Gastric adenocarcinoma90%  Gastric lymphoma 85% 15

16. Barry MarshalRobin Warran 16

17. Heredity Emotional stress Blood group Predisposing factors Active duodenitis or gastritis Gastric metaplasia Producing factors 17

18. Aggravating causes of, and defense mechanisms against, peptic ulceration 18

19.  Any area where pepsin and acid are present  Prevailing locations ◦ Duodenum: duodenal bulb ◦ Stomach: over lesser curvature 19

20.  I type – ulcers of lesser curvature of stomach  II type – combined ulcers of stomach and duodenum  III type – ulcers of prepyloric part stomach  IV type – ulcers of duodenum 20

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22. Gastric ulcer: in the centre of or left to epigastrium Duodenal ulcer: to the right of midline in epigastruim LOCATION Early: 0.5-1 h after meal, duration 1.5-2 hh, in gastric ulcers Late: 1.5-2 hh after meal, in duodenal and pyloric ulcers Nocturnal Pain of “hunger”: 6-7 hh after meal and ceased after meal TIME Burning Gnawing Dull Cramplike CHARACTER Cardiac area Left scapula Thoracic part of spinal column Lumbar region IRRADIATION Antacids Milk Meal After vomiting PAIN RELIEF 22

23. Related with gastroesophageal reflux After meal HEARTBURN More common in gastric ulcers BELCHING At the peak of pain More common in gastric ulcers Pain relief after vomiting NAUSEA & VOMITING Excessive APPETITE 23

24.  Vegetative dystonia: cold, damp palms, mottled skin, bradycardia, hypotension  Palpation: tenderness  Percussion: Mendel’s symptom, succussion splash (gastric outlet obstruction) 24

25.  Non-complicated PUD – service of 1 st category  Complicated PUD – service of 2 nd category  Services of 3.1 category: ◦ Professional examination ◦ Interpretation of clinical and biochemical tests ◦ CBC ◦ Gastric lavage ◦ Diet prescription  Services of 3.2 category: ◦ Analysis of gastric juice and duodenal contents ◦ Ultrasound ◦ Endoscopy ◦ Radiologic examination ◦ Biopsy  Services of 4 category: ◦ Rational nutrition ◦ Struggle with harmful habits ◦ Personal hygiene 25

26. CBC ↑Hb ↑Erythrocyte Secretory function of stomach ↑BAO (N=5 mmol/h) ↑MAO (N=18-26 mmol/h) Occult blood feces analysis Latent PUD Exacerbation Stomach cancer Endoscopy Round or oval Edges: sharp, hyperemic, edematous X-ray (Barium meal) Niche sign Retention of barium meal Duodenogastric reflux Fold convergence Local spasm of stomach *BAO – basal acid output *MAO – maximal acid output 26 Biopsy Test with Insulin Test with Histamine pH meter Gastrin concentration in serum

27.  Invasive( through endoscopy) ◦ Gastric biopsy and staining ◦ Culture of biopsy specimen ◦ Tests using urease enzyme in biopsy specimens  Non-invasive: ◦ Urea breath test ◦ H.pylori antibodies ◦ Stool antigen ◦ Salivary antigen 27

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36.  Haemorrhage  Perforation  Penetration (pancreas, liver)  Pyloric stenosis (due to scarring)  Malignization 36

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38.  Hematemesis  Melena  Bergman’s symptom 38

39. I STAGE Actively bleeding ulcer II STAGE Signs of stopped fresh haemorrhage Thrombosed vessels at the bottom of ulcer Clot of blood III STAGE Absence of bleeding apparent signs 39

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42. Compensation 1-0.5 cm Subcompensation 0.5-0.3 cm Decompensation <0.3 cm 42

43.  Neoplasm of the stomach  Pancreatitis  Pancreatic cancer  Diverticulitis  Nonulcer dyspepsia (also called functional dyspepsia)  Cholecystitis  Gastritis  MI—not to be missed if having chest pain 43

44.  Diet №1: white stale bread, vegetable soups, softly boiled porridge, potato mash, fish, birds, mature fruits, berry and fruit juices, cottage cheese, milk, omelette, pudding  Banned: spicy foods, marinated and smoked products  Frequent small meals: 6-7 times a day 44

45.  H.pylori supressors:  H.pylori supressors: De-nol, Metronidazole, Furazolidone, Oxacillin, Amoxycillin  Antisecretory drugs M-anticholinergic drugs: Nonselective: Atropine, Platyphyllin, Methacin Selective: Gastrozepine, Pirenzepine H2-histamine receptor blockers: Cimetidine, Ranitidine, Famotidine Proton pomp inhibitors: Omeprazole, Lansoprazole, Rabeprazole Antagonists of gastrin receptors: Milid, Proglumide Antacids: Magnesium hydroxide, Aluminum hydroxide, Almagel, Maalox 45

46.  Gastrocytoprotectors Cytoprotectors that stimulate mucus production: Carbenoxolone, synthetic prostaglandins (Enprostile, Misoprostole) Cytoprotectors that form protective film: Sucralfate, colloid bismuth (De-nol), Smecta Astringents: Vicaline, Vicair  Drugs that normalize motor function of stomach and duodenum  Drugs that normalize motor function of stomach and duodenum (Metoclopramide), spasmolytics (Papaverine, No-spa) 46

47.  H2-blockers: gynecomastia, impotence  Aluminum hydroxide: constipation  Magnesium hydroxide: diarrhea 47

48.  De-nol 1 tablet 3 times/day, 4-6 weeks  Clarythromycin 250 mg, 2 times/day, 7-10 days  Metronidazole 250 mg, 4 times/day, 14 days 48

49.  De-nol [4-6 weeks] + Metronidazole [10-14 days]  De-nol [4-6 weeks] + Tetracyclin OR Amoxycillin [10 days]  Amoxycillin OR Clarythromycin [7- 10 days] + Omeprazole [40 mg, 4-6 weeks] 49

50.  De-nol [4-6 weeks] + Metronidazole [10-14 days] Tetracyclin [7-10 days]  Omeprazole + Amoxycillin OR Clarythromycin + Metronidazole  Metronidazole [10-14 days] + Amoxycillin [10 days] + Ranitidine [150 mg, 10-14 days] 50 A week

51. Omeprazole + De-nol+ Amoxycillin OR Clarythromycin + Metronidazole 51 10 days

52. PRIMARY Revelation and elimination of risk factors Sanitary and prophylactic measures SECONDARY Early diagnosis and timely treatment Screening, professional examination, questionnarires TERTIARY Prevention of complications 52

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