1. Tashkent Medical Academy
Peptic Ulcer Disease

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

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

5. Microscopic section of a gastric gland

6. Cells 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

7. Components involved in providing gastroduodenal mucosal defense and repair

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

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

10. 1 – submucosa
2 – hard, undermined margin

11. Peptic Ulcers: Gastric & Dudodenal

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

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

14. Etiology
Helicobacter pylori
NSAIDs (aspirin)

15. H.pylori in GI diseases Healthy subjects 20-50%
Chronic active gastritis %
Duodenal ulcer >90%
Gastric ulcer %
Gastric adenocarcinoma 90%
Gastric lymphoma %

16. Barry Marshal
Robin Warran

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

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

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

20. Johnson’s classification (according to site, clinical manifestations)
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

21. Forms (according to severity)
Mild
1 time/year
Exacerbations
Easily treated
Few symptoms
Medium-severe
2-3 times/year
Treated by full course therapy
Severe
Frequent exacerbations
Absence of stable remission
Evident clinical manifestation

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

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

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

25. GP in Uzbekistan Non-complicated PUD – service of 1st category
Complicated PUD – service of 2nd 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

26. Laboratory and instrumental examination
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
(Barium meal)
X-ray
Niche sign
Retention of barium meal
Duodenogastric reflux
Fold convergence
Local spasm of stomach
*BAO – basal acid output
*MAO – maximal acid output
Biopsy
Test with Insulin
Test with Histamine
pH meter
Gastrin concentration in serum

27. Diagnosis of Helicobacter pylori infection
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

28. Radiology in PUD

29. Duodenal Ulcer

30. Peptic Ulcers: Gastric & Dudodenal

31. Gastric ulcer in endoscopy

32. Gastric ulcer

33. Gastric erosions

34. Duodenal ulcer

35. Duodenal ulcer

36. 20% Complications Haemorrhage Perforation
Penetration (pancreas, liver)
Pyloric stenosis (due to scarring)
Malignization
20%

37. Haemorrhage

38. Haemorrhage
Hematemesis
Melena
Bergman’s symptom

39. Stages of bleeding by Forrest (endoscopy)
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

40. Ulcer perforation

41. Gastric outlet stenosis

42. Stages of stenosis Compensation 1-0.5 cm Subcompensation 0.5-0.3 cm
Decompensation
<0.3 cm

43. Differential Diagnosis
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

44. Treatment – Medical nutrition
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

45. Treatment - Drugs
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

46. Treatment - Drugs 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 (Metoclopramide), spasmolytics (Papaverine, No-spa)

47. Side effects of drugs H2-blockers: gynecomastia, impotence
Aluminum hydroxide: constipation
Magnesium hydroxide: diarrhea

48. Therapy regimens MONOTHERAPY
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

49. Therapy regimens DOUBLE THERAPY
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]

50. Therapy regimens TRIPLE THERAPY
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, days]
A week

51. Therapy regimens QUADRUPLE THERAPY
Omeprazole + De-nol+ Amoxycillin OR Clarythromycin + Metronidazole
10 days

52. Prophylaxy 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

53. To avoid sickness, eat less; to prolong life, worry less. Chu Hui Weng

54. THANKS FOR YOUR ATTENTION AND PATIENCE!!!