PEPTIC ULCER DISEASE Lykhatska G.V.

1. PEPTIC ULCER DISEASELykhatska G.V.

2. Peptic ulcer disease - Is recurrent disease, the main feature of which is the formation of defects (ulcers) of the stomach mucosa and / or duodenal mucosa, which penetrates to mucosal layer, submucosa and deeper, unlike erosion

3. Definition • Ulcers may range in size from several millimeters to several centimeters. • Ulcers are delineated from erosions by the depth of penetration; erosions are more superficial and do not involve the muscularis mucosae.

4. ETIOLOGY of peptic ulcer disease • 1. Helicobacter pylori • 2. NSAIDS • 3. Heredity • 4. Smoking • 5. Association with other diseases or known factors

6. Zollinger-Ellison syndrome Clinical manifestation hypergastrinaemia caused gastrynoma: gastrin-producing tumor (1 or more) of the pancreas, colon, duodenum , peripancreatic lymph nodes, G-cells of the gastric mucosa (triangle gastrin) Spread 2.1 cases / 500 000 60-80% of cases - benign 1% of gastroduodenal ulcers Gastrin> 100ph/ml (N), 500-1000ph/ml

8. Helicobacterpylori • It is the most important factor in peptic ulcer disease. • It causes 90-96% of duodenal ulcers and 70-80% of gastric ulcers.

9. Etiology: • Helicobacter pylori infection. • Hyperacidity - eg. zollinger ellison. • Drugs - anti-inflammatory (NSAIDs) & Corticostroids. • Cigarette smoking, Alcohol, • Rapid gastric emptying • Personality and stress

10. Helicobacter pylori: • Most common infection in the world (20%) • 10% of men, 4% women develop PUD * • Positive in 70-100% of PUD patients. • H.pylori related disorders: • Chronic gastritis – 90% • Peptic ulcer disease – 95-100% • Gastric carcinoma – 70% • Gastric lymphoma • Reflux Oesophagitis. • Non ulcer dyspepsia

12. NSAIDS Aspirin and other non steroidal anti inflammatory agents damage the gastric mucosal barrier and are an important etiologic factor in 30% cases of gastric ulcer.

13. PATHOGENESIS

15. I. Phase of disease: -Acute -Uncomplete remission -Remission II. Course of disease: -mild -moderate - severe. III. Localization: -stomach -duodenum -stomach + duodenum -gastroeneroanostomosis IV.Association with Helicibacter pylori: - H. pylori – associated - H. pylori – not associated V. Complications -Hemorrhage -Perforation -Penetration -Pyloristenosis -Malignancy Classification

16. Example of diagnosis • Peptic ulcer disease, acute phase, mild course, active ulcer of duodenum, H. pylori – associated.

17. CLINICAL AND INSTRUMENTAL SYNDROMES • Pain syndrome • Dyspeptic syndrome:- nausea - vomiting - heartburn - eructation - constipation • Asthenic syndrome • Syndrome of endoscopic changes • Syndrome of roentgenographical changes

18. CLINICAL FEATURES PAIN • Site: Epigastrium Mendel’s symptom “+”

19. Character: Burning in character • Radiation: Pain is localised and patient is able to point it with his one finger "pointing sign". If pain is radiating to the back in inter scapular region and not responding to antacids or other anti-ulcer drug, suggests posterior penetration of ulcer into the pancreas. • Time of pain: Soon after eating within 15-30 minutes in gastric ulcer while 2-3 hours after eating in duodenal ulcer that frequently awakens the patient at night. • Relation with food: Patient with gastric ulcer are afraid to eat because it causes pain due to release of acid in response to food. Patients with duodenal ulcer feel pain in empty stomach and get relief after taking food which causes partial neutralization of acid. Then in response to food there is increased acid secretion which causes pain after 2-3 hours. Acid induced pain is believed due to acid stimulation of chemical receptors.

20. Endoscopy: • Endoscopyis the procedure of choice for diagnosis of peptic ulcer • All patients with gastric ulcer require biopsy initially and the follow up endoscopy and biopsy after 6 weeks of starting therapy, to confirm that the ulcer has healed.

21. PEPTIC ULCER DISEASE

22. PLAN of INVESTIGATIONS • Total blood count • Biochemical analysis • Urinanalysis, Diastase of urine • Coprogram • Hidden blood in feces • ECG • Endoscopy+biopsy+ Histology • Diagnosis of HP infection • X-ray • USD • pH-metry

23. ENDOSCOPY

25. Gastric ulcer (posterior wall)

26. Gastric ulcer(angle of stomach)

27. Duodenal ulcer (anterior wall of duodenal bulb)

28. Duodenal ulcer (posterior wall of duodenal bulb)

29. Duodenal ulcer (middle part, anterior wall, 9-12 mm)

30. Duodenal ulcer

31. GASTRIC CANCER(endoscopy)

32. Barium meal (double contrast technique) • Barium meal is less commonly used now. • It also reveals gastric and duodenal ulcers.

33. Upper GI series in which doublecontrast (barium and air) is used, showing roundedcollection of barium in an ulcer (arrow) in the duodenalbulb of a patient presenting with dyspepsia(uncomplicated duodenal ulcer)

35. Histology • H. pylori can be detected histologically on biopsy of gastric mucosa obtained at endoscopy and stained with haematoxylin and eosin.

36. Noninvasive method carbon urea breath test : Breathing tests with labelled 13C (the "gold standard") and 14C carbon atoms "Helik" - test Serum (immunological) methods: determination of serum IgG, IgA; rapid tests using capillary blood from immunoprecipitation reactions Molecular biological methods based on PCR (material for research: saliva, plaque, urine, feces) Stool test - definition of Hp antigen in stool

37. Urea breath test with I3C • This is a quick and easy way of detecting the presence of H. pylori by urease production with release of labelled CO2 detected on a mass spectrometer. • This test indicates active infection but is expensive.

39. COMPLICATIONS • Hemorrhage • Perforation • Penetration • Pylorostenosis • Malignancy

41. PERFORATIONDiagnosis is confirmed if an upright or a lateral decubitus x-ray of the abdomen shows free air under the diaphragm or in the peritoneal cavity, but the diagnosis is not excluded if no air is seen.

42. Penetration - penetration ulcers contiguous organ tissues which are its bottom (30-35% of all complications). the head of the pancreas liver gall bladder omentulum liver, duodenum ligament

43. Gastric outlet obstruction • Symptoms include recurrent large volume vomiting, occurring more frequently at the end of the day and often as late as 6 h after the last meal.

44. Gastric outlet obstruction

46. Treatment of PUD • ANTIBIOTICS (Clarithromycin, Amoxycillin) • ANTISECRETORY DRUGS: - PROTON PUMP INHIBITORS - H2 RECEPTOR ANTAGONISTS - ANTACIDS(Almagel, Maalox) • GASTROCYTOPROTECTORS • DRUGS, WHICH IMPROVE MOTOR FUNCTION OF STOMACH (Cerucal, Motilium, Eglonil); • SPASMOLYTICS

47. PROTON PUMP INHIBITORS • These drugs are also called H+, K+ ATFase inhibitors. • Compared with H2 receptor antagonists, proton pump inhibitors provide faster pain relief and more rapid ullcerhealing. • They are the most powerful inhibitor of gastric secretion yet discovered. • They inhibit over 90% of 24 hour acid secretion while H2 blocker less than 65% in standard dosages. • They are also used in combination therapy for eradication of Helicobacter pylori

49. ANTACIDS(Almagel, Maalox) • Antacids promote ulcer healing through stimulation of gastric defense mechanism. • Due to availability of other potent antiulcer drugs they are not used as first line agents in the treatment of acute ulcers.