Peptic & Duodenal Ulcer.pptx

For 2nd year B.Sc Nursing students

1. PEPTIC & DUODENAL ULCER Presented By : Mr . Nandish. S Asso . Professor Mandya Institute of Nursing Sciences

2. Definition: It is a condition characterized by erosion of the GI Mucosa resulting from the digestive action of HCl and pepsin. It is an excavation that forms in the mucosa of stomach, pylorus, duodenum or esophagus . They are open sores that develop on the inside lining of stomach or upper part of small intestiine . Any part of GI Tract that comes in contact with gastric secretions are susceptible for ulcer development. Erosion may extend as deeply as muscle to the peritoneum.

3. Incidence : 4.72 % of indian population are suffering from ulceration. 6 to 7 million people in the world are facing this problem every year. 10% of Males & 4% of females are found victims of PUD. Rate of incidence is high in the 5 th decade of men.

4. Types : They can be classified as acute or chronic depending on the degree and duration of mucosal involvement. Acute is associated with superficial erosion and minimal inflammation. It is of short duration & resolves quickly when the cause is identified. Chronic is one of the long duration eroding through the muscular wall. It is present continuously for many months or intermittently through out person’s lifetime.

5. Particulars Gastric Ulcer Duodenal ulcer Lesion Superficial, smooth margin, round, oval or cone shaped. Penetrating, associated with deformity of duodenal bulb. Location Predominantly Antrum , also seen in body & Fundus First 1 – 2 cm of duodenum Incidence Greater in women. Peak 50 – 60 yrs Greater in men, increasing in women after menopause. Recurrence rate & complication High Hemorrhage , Perforation, outlet Obstruction High Hemorrhage , Perforation, outlet Obstruction

6. Etiology : H.Pylori infection : it secretes urease which is suitable for its survival. It generate ammonia in mucous layer, that render mucosa for vulnerable activities. NSAID’s (Aspirin) : they block function of Cyclo-oxygenase 1, which is essential for production of prostaglandins. (they help in protection of gastric mucosa from gastric acid) Stress : they develop pfollowing major physiologic insult such as complicated Surgery, Burns, severe Trauma or Hypotension. (Physiologic stress Ulcers)

7. - Dietary Factors : Spicy food consumption Caffeine & Coffee can cause or exacerbate ulcers Alcohol consumption and smoking Other Factors: Gastric ischemia Metabolic disturbances CMV (Cytomegalovirus) Upper Abdominal Radiotherapy

8. Pathophysiology

9. Clinical Manifestations : Gastric & duodenal mucosa is not rich in sensory pain receptors, which account for no pain. If pain occurs, it is described as “Burning or cramp like” which is located in midepigastric region. Pain usually occur when the stomach is empty and also 1 – 2 hours after the meals.

10. Diagnostic studies : History collection & Physical examination H. Pylori testing of breath, urine, blood, tissue Upper GI Endoscopy with biopsy Upper GI Barium contrast study Complete Blood Count Urinalysis LFT Serum Electrolytes

11. Complications : There are three Major complications & all are considered emergency situations. Hemorrhage : it develops from erosion of ulcer through major blood vessel & it accounts for GI Bleeding. Perforation : are due to large penetrating duodenal ulcers & located on posterior mucosal wall. It is more lethal. Gastric outlet Obstruction

12. TREATMENT : Aim : to decrease the degree of gastric acidity, enhance mucosal defense mechanism & minimise the harmful effects on mucosa. Regimen : Adequate Rest Dietary modifications Drug therapy Elimination of smoking Long term follow up care.

13. Categories Medications Antisecretory Drugs H2 Secretory Blockers : Cimetidine, Ranitidine, Famotidine, Nizatidine Proton Pump Inhibitors : Omeprazole, Lansoprazole , Pantoprazole. Anti secretory Drugs Misoprostol Cytoprotective Sucralfate , Bismuth subsalicylate Neutralizing Drugs Antacids (Aluminium hydroxide gel, calcium carbonate) Antibiotics Amoxicillin, Metronidazole, Tetracycline , Clarithromycin Others Tricyclic Antidepressants – imipramine, doxepin

14. NPO NG Suction Complete bed rest Fluid replacement Gastric lavage Bland diet (six meals in a day) Cessation of smoking Blood transfusion

15. Surgical Therapy : Surgery is indicated during intractability, history of hemorrhage , pyloric ulcers, multiple ulcer sites, drug induced ulcers, malignant ulcer & obstruction. Procedures performed are Partial Gastrectomy Vagotomy Pyloroplasty

16. Partial Gastrectomy with removal of distal 2/3 rd of stomach and anastomosis of the gastric stump to the duodenum is called G astroduodenostomy or B illroth I Operation.

17. Partial G astrectomy with removal of distal 2/3 rd of the stomach and anastomosis of gastric stump to the jejunum is called gastrojejunostomy or Billroth II Operation.

18. Vagotomy is the severing of the vagus nerve either totally or selectively at some point in its innervation to the stomach. In truncal vagotomy , both anterior & posterior trunks are severed. In selective vagotomy , a particular branch of vagus nerve is severed. Pylroplasty consists of surgical enlargement of the pyloric sphincter to facilitate the easy passage of contents from the stomach. A pyloroplasty accompanying vagotomy increase gastric emptying.

19. Postoperative complications : Dumping syndrome (it stimulates intestinal motility and urge to defecate) Postprandial hypoglycemia : it results due to uncontrolled gastric emptying of the bolus of fluid high in carbohydrate into the small intestine. Bile reflux gastritis : prolonged contact of bile causes damage to the gastric mucosa.

20. Nursing Management : Acute pain, related to increased gastric secretions Perforation of GI Mucosa related to impaired mucosal tissue integrity. Hemorrhage related to eroded mucosal tissue Nausea related to acute exacerbation of disease Ineffective therapeutic regimen management related to lack of knowledge of long term management.

21. THANK YOU