1. PEPTIC ULCER DISEASE

2. INTRODUCTION 3. PREVELENCE In India, the prevalence of peptic ulcers is estimated to be 4-10 per1000 population 4. INCIDENCE Age 3060 Male: female3:1 5. RISK FACTORS H. pylori, Alcohol, Smoking, Cirrhosis, Stress Usually 50 and over Male higher risk Normal ,hyper secretion of stomach acid (HCl) (zollinger Ellison syndrome) Gastritis, Use of NSAIDs 6. Types Acute Chronic 7. Acute Is associated with superficial erosion and minimal inflammation it is of short duration and resolves quickly when the cause is identified and removed 8. Chronic 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 persons life time 9. Another classification Gastric duodenal 10. Comparison of gastric and deodenal ulcer Gastric ulcers Duodenal ulcers Lesion Superficial smooth margins ,not oval or cone shaped Penetrating Associated with deformity of duodenum from recurrent healing Location of lesion Predominantly antrum also in body and funds First 1-2 cm of duodenum Gastric secretion Normal or decreased increased Incidence Greater in women Peak age 50-60 yrs Common in lower socio economic status ,increased with smoking use of drug use and alcohol use seen in pyloric sphincter and bile reflex Greater women Post menopausal women higher risk Associated with pyloric stress Increased with smoking alcohol and drug use associated with other disease COPD ,zollinger Ellison syndrome chronic renal failure Clinical manifestation Burning or gacious pressure in high left epigastriam and back and upper abdomen ,pain 1-2 hrs after meal ,if penetrating ulcer aggravation of discomfort with food occasional nausea and vomiting Burning,cramping pressure like pain back pain Recurrence rate high high 11. ETIOLOGY 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 tumors Esophageal ulcers GERD 12. PATHOPHYSIOLOGY 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. 13. CLINICAL MANIFESTATIONS 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 14. ASSESSMENT AND DIAGNOSTIC FINDINGS Pain, Epigastric tenderness, Abdominal distention. A barium study Stools study Gastric secretory studies H. Pylori infection Breath test that detects H. Pylori 15. MEDICAL MANAGEMENT Antibiotics Eradicate H. pylori Rest sedatives Tranquilizers Octreotide (decrese gastric activity) cytoprotective agents (sucralfate) 16. PHARMACOLOGIC THERAPY proton pump inhibitors antibiotics bismuth salts histamine 2 antagonist proton pump inhibitors 17. STRESS REDUCTION AND REST Avoid stressful or exhausting situations A rushed lifestyle irregular schedule Biofeed back Hipnosis Behavier modification Change in job 18. SMOKING CESSATION smoking decreases the secretion of bicarbonate from the pancreas into the duodenum resulting in increased acidity of the duodenum. 19. DIETARY MODIFICATION avoiding extremes of temperature Over stimulation from consumption of meat extracts alcohol, coffee (including decaffeinated coffee) Milk cream 20. SURGICAL MANAGEMENT Principles of surgery Reduce acid secreting ability Remove malignant or potentially malignant lesions treat surgical emergency Treat clients do not respond to medical intervention 21. VAGOTOMY 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 22. Truncal 23. VAGOTOMY WITH PYLOROPLASTY 24. GASTROENTEROSTOMY 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 25. ANTRECTOMY 26. SUBTOTAL GASTERCTOMY 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 27. BILLROTH GASTRECTOMY Operation was devised more by accident than a 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 28. BILROTH 1 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 29. BILROTH 1 30. BILROTH II 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 31. BILROTH II 32. COMPLICATIONS 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 33. Late dumping 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 34. TREATMENT The principal treatment is dietary manipulation, dry meals are best, and avoiding fluids with a high carbo- hydrate content 35. Other side effects Hemorrhage Marginal ulcers Alkaline reflex gastritis Nutritional deficiency ( Vitamin B12 and folic acid deficiency) 36. FOLLOW-UP CARE 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) 37. NURSING PROCESS: Assessment Pain, (type timing, duration) Use of antacids Vomitus Smoking Use of alcohol Use of NSAID Eating habbits , Blood in stool Physical examination 38. NURSING DIAGNOSES 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 39. NURSING INTERVENTIONS RELIEVING PAIN REDUCING ANXIETY MAINTAINING OPTIMAL NUTRITIONAL STATUS MAINTAINING OPTIMAL NUTRITIONAL STATUS TEACHING PATIENTS SELF-CARE 40. RELIEVING PAIN Pain relief can be achieved with prescribed medications. The patients hould avoid aspirin, foods and beverages that contain caffeine, and decaffeinated coffee, meals should be eaten at regularly paced intervals in a relaxed setting. Some patients benefit from learning relaxation techniques to help manage stress and pain and to enhance smoking cessation efforts 41. REDUCING ANXIETY The nurse assesses the patients level of anxiety. Patients with peptic ulcers are usually anxious, but their anxiety is not always obvious. Appropriate information is provided at the patients level of understanding, all questions are answered, and the patient is encouraged to express fears openly. Explaining diagnostic tests and administering medications on schedule also help to reduce anxiety. The nurse interacts with the patient in a relaxed manner, helps identify stressors, and explains various coping techniques and relaxation methods, such as biofeedback, hypnosis, or behavior modification. The patients family is also encouraged to participate in care and to provide emotional support. 42. MAINTAINING OPTIMAL NUTRITIONAL STATUS assesses the patient for malnutrition and weight loss. After recovery from an acute phase of peptic ulcer disease, the patients are advised about the importance of complying with the medication regimen and dietary restrictions. 43. TEACHING PATIENTS SELF-CARE Give information about medications to be taken at home, including name, dosage, frequency, and possible side effects, stressing the importance of continuing to take medications even after signs and symptoms have decreased or subsided. the patient is instructed to avoid certain medications and foods that exacerbate symptoms as well as substances that have acid producing potential (eg, alcohol; caffeinated beverages such as coffee, tea, and colas). It is important to counsel the patient to eat meals at regular times and in a relaxed setting, and to avoid overeating the nurse also informs the patient about the irritant effects of smoking on the ulcer and provides information about smoking cessation programs. The nurse reinforces the importance of follow-up care for approximately1 year, the need to report recurrence of symptoms, and the need for treating possible problems that occur after surgery, such as intolerance to dairy products and sweet foods 44. POTENTIAL COMPLICATIONS Hemorrhage Perforation and Penetration Pyloric Obstruction 45. Hemorrhage 1) Monitoring the hemoglobin and hematocrit to assist in evaluating blood loss 2) Inserting an NG tube to distinguish fresh blood from coffee grounds material, to aid in the removal of clots and acid, to prevent nausea and vomiting, and to provide a means monitoring further bleeding 3) Administering a room-temperature lavage of saline solution or water. This is controversial; some authorities recommend using ice lavage 4) Inserting an indwelling urinary catheter and monitoring urinary output 5) Monitoring vital signs and oxygen saturation and administering oxygen therapy 6) Placing the patient in the recumbent position with the legs elevated to prevent hypotension; or, to prevent aspiration from vomiting, placing the patient on the left side 7) Treating hemorrhagic shock 46. Perforation and Penetration Hypotension and tachycardia, indicating shock Because chemical peritonitis develops within a few hours after perforation and is followed by bacterial peritonitis, the perforationmust be closed as quickly as possible and assesses the patient for peritonitis or localized infection (increased temperature, abdominal pain, paralytic ileus, increased or absent bowel sounds, abdominal distention). Antibiotic therapy is administered parenteral as prescribed Immediate surgical repair and haemodynamic stabilisation 47. Pyloric Obstruction insert an NG tube to decompress the stomach. Confirmation that obstruction is the cause of the discomfort is accomplished by assessing the amount of fluid aspirated from the NG tube. A residual of more than 400 mL strongly suggests obstruction . Usually an upper GI study or endoscopy is performed to confirm gastric outlet obstruction. Decompression of the stomach and management of extracellular fluid volume and electrolyte balances may improve the patients condition and avert the need for surgical intervention. A balloon dilatation of the pylorus via endoscopy may be beneficial. If the obstruction is unrelieved by medical management, surgery (in the form of a vagotomy andantrectomy or gastrojejunostomy and vagotomy) may be required. 48. FOLLOW-UP CARE Recurrence within 1 year may be prevented with the prophylactic use of H2 receptor antagonists given at a reduced dose. all patients require maintenance therapy; it may be prescribed only for those with two or three recurrences per year, 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) etc 49. Evidence based practice Conclusion 50. Bibliography 51. Thank you