Peptic ulcer disease

Diagnosis and management of peptic ulcer disease

1. PEPTIC ULCER DISEASE DR. AJAY KUMAR MKCG,MCH

2. AIM OF DISCUSSION Anatomy of Stomach Physiology of Stomach Definition of PUD Aetiology of PUD Types of PUD Symptoms Treatment and Complications.

3. ANATOMY OF STOMACH Stomach is a J-shaped organ in upper lt. region of abdominal cavity. In adult life , Stomach is located between T10 to L3 vertebrae. It is the dilated part of alimentary canal between oesophagus and duodenum It is divided into 4 parts : - CARDIA - FUNDUS - BODY (CORPUS) - PYLORIC ANTRUM

4. Cont…. SURFACES :- Antero-superior surface Postero-inferior surface OPENINGS :- Gastro-oesophagus – From oesophagus Pyloric – To duodenum

5. Cont.. LAYERS OF STOMACH:- Mucosa Submucosa Muscle layers - Oblique muscle - Circular muscle - Longitudinal muscle Serosal layer

6. BLOOD SUPPLY

7. VENOUS DRAINAGE

8. LYMPHATIC DRAINAGE

9. NERVE SUPPLY SYMPATHETIC T6 to T10 spinal segments Motor to pyloric sphincter Carry pain sensation from stomach PARASYMPATHETIC Vagus nerve & its branches Gastric motility Gastric secretion

10. MICROSCOPIC ANATOMY Gastric glands: Mucous glands- Located at cardia and secrets mucous. Chief cells – Secrets pepsinogen and stimulated by Vagus. Parietal cells- Secrets HCl and Intrinsic factor and stimulated by Ach, Gastrin, Histamine. Gastrin cells – Located at distal part, secrets Gastrin and stimulated by Amino acids. D cells- Secrets Somatostatin which inhibits gastric emptying, pancreatic secretion and GB contraction.

11. PHYSIOLOGY OF STOMACH FUNCTION OF STOMACH : - Reservoir for food Digestion Gastric acid production Slows food entering into duodenum Absorption of VitB12

12. Stomach contains a number of biologically active peptides in nerves and endocrine cells. These are :- - Gastrin - Somatostatin - Vasoactive intestinal peptides (VIP ) - Substance P

13. GASTRIN Produced by G- cell Synthesized as prepropeptide and undergo post translational processing to produce biologically active Gastrin. Stimulus for secretion are :- - Amino acids produced from proteolysis - Gastric distention due to food - Lumen pH>3.

14. Inhibitors of Gastrin secretion : - Somatostatin - Lumen Ph<3 Action of Gastrin :- Act on parietal cells to secrets HCl in gastric phase Once gastric distention decreases, there is stimulation of Somatostatin occurs and attenuating Gastrin secretion.

15. SOMATOSTATIN It is produced by D-cell. It is a 14 amino acid peptide. Actions :- - Inhibits parietal cell acid secretion directly. - Inhibition of Gastrin release. - Downregulation of Histamine release from ECL cells. Stimulator :- lumen Ph<3. Inhibitors :- Ach.

16. HISTAMINE It plays important role in gastric acid secretion by stimulating parietal cells. It is stored in acidic granules of ECL cells and Mast cells. Stimulator :- -Gastrin - Ach - Epinephrine. Inhibitor :- Somatostatin.

17. GHRELIN It is a 28 amino acid peptide. Produced by endocrine cells of the oxyntic mucosa of the stomach. Some amounts from bowel, pancreas. It enhances appetite and increase food intake. It promotes glycolysis and prevent fatty acid oxidation. Used in treatment and prevention of obesity.

18. COMPOSITION OF GASTRIC SECRETION Approx. secretion of gastric juice is 1.5 – 2 liter per day When meal is consumed, it stimulates release of gastric juice from gastric glands. Contain water and solutes. Solutes are inorganic and organic HCL Pepsin Sodium intrinsic factor potassium gastric lipase bicarbonate

19. GASTRIC ACID SECRETION

20. Basolateral membrane of parietal cells contain specific receptors for three major stimulant of acid production. These are :- - Histamine - Gastrin - Ach Each stimulant have their own 2 nd messenger .

21. PHASES OF GASTRIC ACID SECRETION Cephalic phase Gastric phase Intestinal phase

22. CEPHALIC PHASE It occurs even before food enters the stomach It results from sight, smell, thought of food. It accounts for 30% of gastric secretion. Neurogenic signal transmit through vagus nerve (dorsal motor nuclei).

23. GASTRIC PHASE Once food enters the stomach, it excites local enteric reflex, gastrin mechanism, which causes stimulation of gastric juice secretion. It accounts for 60% of gastric secretion. Gastrin is the most important mediator. Ends when antral mucosa is exposed to acid as the gastrin release stops and somatostatin release is increased.

24. INTESTINAL PHASE Presence of food in duodenum or upper part of small intestine, stimulate stomach to secrete small amount of gastric juice. This is due to release of gastrin in duodenal mucosa. It accounts of 10% of gastric secretion.

25. REGULATION OF GASTRIC ACID SECRETION Stimulated by – acetylcholine, gastrin, histamine. Inhibited by- - presence of food in small intestine. - presence of acid, fat, protein breakdown product. - secretin. - gastric inhibitory peptides - VIP - somatostatin

26. GASTRIC MOTILITY AND EMPTYING When food enters stomach the fundus and upper part of body relax and accommodate the food. Peristalsis begins in the lower portion of body, mixing and grinding the food and permitting chyme pass through pylorus and enter the duodenum. In regulation of gastric emptying the antrum, pylorus, upper duodenum function as unit. Contraction of antrum is followed by sequential contraction of the pyloric region and duodenum.

27. REGULATION The rate at which the stomach empties into duodenum depends on the type of food ingested. Food rich in carbohydrate empties fast Protein rich food leaves slowly. And fat containing food leaves stomach very slowly. The rate of emptying also depends on osmotic pressure of the chyme. CCK is also an inhibitor of gastric emptying.

28. PACEMAKER OF GASTRIC PERISTALSIS The source of myogenic activity in GIT has been tracked down to INTERSTITIAL CELLS OF CAJAL , which act as pacemaker, that generates slow wave in smooth muscle.

29. PEPTIC ULCER DISEASE DEFINITION - It is a sore or disruption in the lining of stomach and duodenum. - Peptic refers to Pepsin , a stomach enzyme that breakdown protein. - An ulcer occurs when the lining of stomach and duodenum is corroded by acidic digestive juice secreted by stomach cells.

30. LOCATION : - Stomach - Duodenum - GE Junction - Jejunum

31. TYPES OF PEPTIC ULCER 1. DEPENDING ON THE SITE :- Duodenal Ulcer :- Typically occurs in 1 st inch of 1 st part of duodenum Gastric Ulcer :- Occurs in the lesser curvature Combined

32. 2. DEPENDING ON THE DURATION :- Chronic peptic ulcer Acute peptic ulcer

33. RISK FACTORS H. Pylori infection Use of NSAIDs or Corticosteroid. Smoking Alcohol Physical stress Family history of PUD Increased salivation (water brash). Gastrinoma (ZE Syndrome)

34. PATHOPHYSIOLOGY H. PYLORI :- It is a gram –ve, spiral shaped organism. Lophoflagellate, so moves rapidly in gastric lumen. It uses an adhesion molecule (Bab A) to bind to the Lewis A Ag on epithelial cells. Transmission route is via gastric refluxate.

35. It produces Urease enzyme which cause breakdown of urea and produces ammonia and thus raising pH . The bacteria stimulate chronic gastritis by provoking local inflammatory response underlying epithelium. Infection occurs in childhood but remain asymptomatic and only few people develop clinical disease.

36. VIRULENCE FACTOR :- Vacuolating cytotoxin A (vacA) => Increase permeability. Cytotoxin associated gene A (cag A) => Apoptosis. Adhesins (BabA). Outer inflammatory protein A (oipA).

37. NSAIDs :- Three patterns of mucosal damage are caused by NSAIDs. These are :- - Superficial erosion -Haemorrhages - Silent ulcers.

38. They acts mainly by inhibiting prostaglandins synthesis. Inhibits enzyme COX1 & COX2. Prostaglandin provide a protective layer over gastric mucosa.

39. SMOKING :- Nicotine increases parasympathetic activity => stimulate G cell and ECL cells => Increased secretion of gastrin and histamine. Increased rate of gastric emptying. Decreased pancreatic bicarbonates secretion Reduce mucosal blood flow. Inhibition of mucosal PGs.

40. ACID PEPSIN VERSUS MUCOSAL RESISTANCE An ulcer forms when there is an imbalance between aggressive and defensive factors. Aggravating Factor :- - ACID (HCl) - PEPSIN Defensive factor :- - MUCOSAL BARRIER

41. CLINICAL FEATURES Epigastric pain (MC) - Gastric ulcer pain is associated or closely followed by meal. - Duodenal ulcer pain is relieved by food. - Duodenal ulcer pain is hunger pain and awaken the pt. at night. - Burning in nature - May radiates to back (consider perforation) Chest discomfort Dyspepsia

42. cont… Anorexia, wt. loss. Nausea and Vomiting Heartburn Haematemesis. Melenae Constipation (rare)

43. INVESTIGATIONS Routine investigations Endoscopy +/- biopsy. H. Pylori detection tests - urea breath test - stool antigen test Radiology - CXR Digital PA view – if perforation is suspected. - Double contrast barium radiography.

44. Cont… Serum Gastrin level – value >200pg/ml is high. Measurement of gastric acid production. USG of abdomen

45. UREA BREATH TEST :- - It is based on urease activity in the stomach. - Urease hydrolyses urea to form ammonia and CO2. - Ingest urea labelled with radioactive Carbon. - Hydrolysis of urea => labelled CO2. - Rapidly absorbed into blood and within a few minutes, appear in breath

46. COMPLICATIONS Bleeding Peptic ulcer. Peptic Perforation. CDU leading to Pyloric Stenosis Intractable PUD ZE Syndrome

47. DIFFERENCE BETWEEN GASTRIC AND DUODENAL ULCER

48. MANAGEMENT AIM OF TREATMENT :- Relief of symptom Heal ulcer Prevent recurrence Prevent complications. H. Pylori eradication.

49. ERADICATION OF H.PYLORI FDA Approved Treatment regimen :- Omeprazole 20mg BD + Clarithromycin 500mg BD + Amoxicillin 1gm BD for 10 days. Lansoprazole 30mg BD + Clarithromycin 500mg BD + Amoxicillin 1 gm BD for 10 days. Bismuth subsalicylate 525mg QID + Metronidazole 250mg QID + Tetracycline 500mg QID for14 days + H2 Receptor antagonist x 4wks.

50. TRIPLE THERAPY Omeprazole 20mg/ Lansoprazole 30mg BD Clarithromycin 500mg BD. Amoxicillin 1gm/ Metronidazole 400mg BD. Given for 14 days followed by PPI for 4-6 wks.

51. Bismuth subsalicylate 2 tab QID + Metronidazole 250mg QID + Tetracycline 500mg QID. Ranitidine bismuth citrate 400mg BD + Tetracycline 500mg BD + Clarithromycin / Metronidazole 500mg BD.

52. QUADRUPLE THERAPY Given with Triple therapy fails. Regimen is :- - Omeprazole 20mg/ Lansoprazole 30mg BD - Metronidazole 250mg QID - Tetracycline 500mg QID - Bismuth subsalicylate 2 tabs QID

53. PROTON PUMP INHIBITORS Disrupt chemical binding in stomach cell to reduce acid production, lessening irritation and allowing ulcer to heal. Drugs include :- - Omeprazole - Rabeprazole - Pantoprazole - Lansoprazole - Esomoprazole

54. H2 – RECEPTOR ANTAGONISTS Commonly prescribed anti-ulcer drugs. It includes :- Cimetidine, Ranitidine, Famotidine. Food and antacid reduces absorption. It acts by blocking Histamine from stimulating acid secreting parietal cells. Reduces gastric acid secretion and prevent stress ulcers.

55. ANTACIDS Work locally in stomach by neutralising gastric acid. Relieve pain and promote healing Reduces the total amount of acid in GI Tract These includes :- - Magnesium hydroxide and aluminium hydroxide. - Sodium bicarbonate. - Calcium carbonate. - Simethicone.

56. Strategies for protecting gastric mucosa from acid

57. MUCOSAL PROTECTIVE AGENTS BISMUTH COMPOUNDS :- Tripotassium dicitratobismuthate Colloidal Bismuth subcitrate. SUCRALFATE :- It is a complex of aluminium hydroxide and sulphated sucrose Act by protecting the mucosa from acid pepsin attack

58. GENERAL MEASURES Avoid cigarette smoking Avoid alcohol Avoid NSAIDs groups of drug. Avoidance of coffee and tea. Uses fibre rich diet. Wash hand after using bathroom and before eating and cooking food.

59. SURGICAL TREATMENT INDICATION FOR SURGERY :- - Peptic Perforation - Haemorrhage - Pyloric stenosis SURGICAL OPTIONS :- - Billroth II Gastrectomy - Gastrojejunostomy - Truncal Vagotomy and drainage.

60. BILLROTH II GASTRECTOMY Two – third of stomach is removed Duodenum stump is closed Stomach anastomosed with jejunum.

61. TRUNCAL VAGOTOMY AND DRAINAGE Section of Vagus nerve, which are critically involved in secretion of gastric acid. Reduces the maximal acid output by 50%