Peptic ulcer disease

1. PEPTIC ULCER DISEASE

2. INTRODUCTION

3. In India, the prevalence of peptic ulcers is estimated to be 4-10 per1000 population PREVELENCE

4. Age 30–60 Male: female–3:1 INCIDENCE

5. H. pylori, Alcohol, Smoking, Cirrhosis, Stress Usually 50 and over Male higher risk Normal hypo secretion of stomach acid ( HCl ) (zollinger Ellison syndrome) Gastritis, Use of NSAIDs RISK FACTORS

6. Acute Chronic Types

7. Is associated with superficial erosion and minimal inflammation it is of short duration and resolves quickly when the cause is identified and removed Acute

8. Chronic ulcer is one of long duration eroding through the muscular wall with the formation of fibrous tissue it may be present continuously for many months or intermittently throughout the person’s life time Chronic

9. Gastric duodenal Another classification

10. stress and anxiety gram-negative bacteria H. pylori Stress Excessesive secretion of HCL Familial tendency Blood group o Use of NSAID Alcohol Excessive smoking Hyperacidity Gastrin secreting malignant tumers Esophagial ulcers GERD ETIOLOGY

11. In addition to the inflammation caused by H.pylori infection, there are certain other factors that contribute to peptic ulcer. Peptic ulcer occurs mainly in the gastro duodenal mucosa because this tissue cannot withstand the digestive action of gastric acid HCl and pepsin. Vagus nerve stimulates the parietal cells to secrete gastric acid. The erosion is caused by the increased concentration or activity of pepsin, or by decreased resistance of the mucosa. A damaged mucosa cannot secrete enough mucus to act as a barrier against HCl . The use of NSAIDs inhibits the secretion of mucus that protects the mucosa . PATHOPHYSIOLOGY

12. dull, gnawing pain or a burning Pain is usually relieved by eating Tenderness pyrosis (heartburn), vomiting, constipation or diarrhea, and bleeding burping vomiting bleeding tarry stools CLINICAL MANIFESTATIONS

13. pain , epigastric tenderness , or abdominal distention . A barium study Stools study . Gastric secretory studies H. pylori infection breath test that detects H. pylori ASSESSMENT AND DIAGNOSTIC FINDINGS

14. Antibiotics Eradicate H. pylori Rest sedatives Tranquilizers Octreotide cytoprotective agents MEDICAL MANAGEMENT

15. proton pump inhibitors antibiotics bismuth salts histamine 2 antagonist proton pump inhibitors PHARMACOLOGIC THERAPY

16. stressful or exhausting . A rushed lifestyle irregular schedule STRESS REDUCTION AND REST

17. smoking decreases the secretion of bicarbonate from the pancreas into the duodenum resulting in increased acidity of the duodenum. SMOKING CESSATION

18. avoiding extremes of temperature overstimulation from consumption of meat extracts alcohol, coffee (including decaffeinated coffee , Milk cream DIETARY MODIFICATION

19. Principles of surgery Reduce acid secreting ability Remove malignant or potentially malignant lesions treat surgical emergency Treat clients do not respond to medical intervention SURGICAL MANAGEMENT

20. Vagotomy is performed to eliminate the acid secreting stimulus to gastric cells Truncal Completely cutting each vagus nerve Selective The surgeon partially severs the nerves to preserve the hepatic and celiac branches Proximal Only paritel cell mass is denerveted VAGOTOMY

21. Truncal

22. VAGOTOMY WITH PYLOROPLASTY

23. Permits regurgitation of alkaline deodenal contents thereby neutralizing gastric acid in this procedure a drain is made on the bottom of the stomach and sewn to an opening made in the jejunum GASTROENTEROSTOMY

24. ANTRECTOMY

25. This is a genetic term referring to any surgery that involves partial removal of the stomach may be performed by either Billroth 1 or Billroth 2 SUBTOTAL GASTERCTOMY

26. Operation was devised more by accident thanà surgery design A gastro enterostomy was performed on a gravely ill patient with a pyloric resection by Christian Aiberl Theociot Billroth . 1829-1894, Professor of Surgery, Vienna, Austria. Anton wolfler . 1850-1917, Professor of Surgery, Prague, The Czech Republic further refined the surgery The first successful gastrectomy was performed by Billroth in January 1881, and Wolfler performed the first gastroenterostomy in the same year BILLROTH GASTRECTOMY

27. The surgeon removes a part of distal portion of the stomach including the andrum the remainder of the stomach is anastomosed to duodenum this combined procedure called gastrodeodenostomy this decreases dumping syndrome BILROTH 1

28. BILROTH 1

29. This involves reanastomosis of the proximal remnant of the stomach to the proximal jejunum pancreatic secretions and bile continue to secrete in jejunum even after surgery surgeons prefer Billroth 2 technique for treatment of duodenal ulcers because recurrent ulcer develops less frequent in this procedure BILROTH II

30. BILROTH II

31. Dumping syndrome Early dumping Early dumping include abdominal and vasomotor symptoms which are found in 5-10%of patients the small bowel is filled with food from stomach which have high osmotic load this lead to shift of fluid to stomach from systemic circulation symptoms are vertigo, tachycardia syncope sweating pallor palpitation diarrhea and nausea etc COMPLICATIONS

32. This is reactive hypoglycemia . The carbohydrate load in the small bowel causes a rise in the plasma glucose level, which, in turn, causes insulin levels to rise, causing a secondary hypoglycemia. This can be easily demonstrated by serial measurements of blood glucose in a patient following a test meal. Other symptoms include epigastric fullness distention discomfort abdominal cramping nausea etc the treatment is essentially the same as for early dumping Late dumping

33. The principal treatment is dietary manipulation, dry meals are best, and avoiding fluids with a high carbo­hydrate content TREATMENT

34. Hemorrhage Marginal ulcers Alkaline reflex gastritis Nutritional deficiency ( Vitamin B12 and folic acid deficiency) Other side effects

35. The likelihood of recurrence is reduced if the patient avoids smoking, coffee (including decaffeinated coffee) and their caffeinated beverages, alcohol, and ulcerogenic medications ( eg , NSAIDs) FOLLOW-UP CARE

36. NURSING PROCESS:

37. Acute pain related to incresed gastric secretions , decresed mucosal protection ,and ingestion of gastric irritants as evidenced by burning cramp like pain in epigastrium and abdomen Nausea related to acute exacerbation of disease process as evidenced by episodes of nausea and vomiting Ineffective therapeutic regimen management related to lack of knowledge of long term management of peptic ulcer disease and consequence of not following treatment plan and unwillingness to modify lifestyle as evidenced by frequent questions about home care incorrect response to questions about peptic ulcer disease NURSING DIAGNOSES

38. Hemorrhage Perforation Penetration Pyloric obstruction (gastric outlet obstruction) POTENTIAL COMPLICATIONS

39. RELIEVING PAIN REDUCING ANXIETY MAINTAINING OPTIMAL NUTRITIONAL STATUS MAINTAINING OPTIMAL NUTRITIONAL STATUS TEACHING PATIENTS SELF-CARE NURSING INTERVENTIONS

40. Hemorrhage Perforation and Penetration Pyloric Obstruction POTENTIAL COMPLICATIONS

41.   Evidence based practice Conclusion

42. Bibliography