Gastric & Duodenal Ulcer Management PDF

Management of Patients With Gastric and Duodenal Disorders Chapter 40 1 LEARNING OBJECTIVES On completion of this chapter, the learner will be able to: 1. Compare the...

Management of Patients With Gastric and Duodenal Disorders Chapter 40 1 LEARNING OBJECTIVES On completion of this chapter, the learner will be able to: 1. Compare the etiology, clinical manifestations, and management of acute gastritis, chronic gastritis, and peptic ulcer. 2. Use the nursing process as a framework for care of patients with peptic ulcer. 3. Describe the pharmacologic, dietary, and surgical treatment of peptic ulcer. 4. Use the nursing process as a framework for care of the patient with gastric cancer or tumors of the small intestine 2  Gastritis Inflammation of the gastric or stomach mucosa, is a common GI problem. It affects women and men about equally and is more common in older adults. Gastritis may be acute, lasting several hours to a few days, or chronic, resulting from repeated exposure to irritating agents or recurring episodes of acute gastritis. Types of gastritis: erosive, nonerosive 3 Gastritis 1.Erosive gastritis: form of acute gastritis is most often caused by local irritants such as aspirin and other nonsteroidal anti- inflammatory drugs (NSAIDs), alcohol consumption. 2. Nonerosive gastritis: is most often caused by an infection with Helicobacter pylori (H. pylori). 4  5 Gastritis Acute gastritis: Caused by the ingestion of strong acid or alkali, the mucosa to become gangrenous or to perforate. Scarring can occur, resulting in pyloric stenosis. Acute gastritis also may develop in acute illnesses, especially when the patient has had major traumatic injuries; burns; severe infection; hepatic, kidney, or respiratory failure; or major surgery (stress-related gastritis). 6  Gastritis Chronic gastritis: Often classified according to the underlying causative mechanism, which most often includes an infection with H. pylori. Chronic gastritis may also be caused by a chemical gastric injury as the result of long-term drug therapy (e.g., aspirin and other NSAIDs) or reflux of duodenal contents into the stomach, which most often occurs after gastric surgery. Autoimmune disorders such as Hashimoto thyroiditis, Addison disease, and Graves’ disease are also associated with the development of chronic gastritis 7 Gastritis Pathophysiology: 1. A disruption of the mucosal barrier that normally protects the stomach tissue from digestive juices (HCL & pepsin). 2. The impaired mucosal barrier allows corrosive HCL, pepsin to come in contact with the gastric mucosa, resulting in inflammation. 3. Inflammation causes the gastric mucosa to become edematous and hyperemic (congested with fluid and blood) and to undergo superficial erosion. 4. Superficial ulceration may occur as a result of erosive disease and may lead to hemorrhage. 5. In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes, and eventually atrophy 8  Gastritis Clinical Manifestations: The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia (indigestion), anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive gastritis may cause bleeding, which may manifest as blood in vomit or as melena (black, tarry stools) or hematochezia (bright red, bloody stools). 9 Gastritis The patient may complain of fatigue, pyrosis (a burning sensation in the stomach and esophagus that moves up to the mouth; heartburn) after eating, belching, a sour taste in the mouth, early satiety, anorexia, or nausea and vomiting. Intolerance to spicy or fatty foods or slight pain that is relieved by eating. Not be able to absorb vitamin B12 because of diminished production of intrinsic factor by the stomach’s parietal cells due to atrophy, which may lead to pernicious anemia. 10  Gastritis Assessment and Diagnostic Findings: Determined by an endoscopy and histologic examination of a tissue specimen obtained by biopsy. A complete blood count (CBC) may be drawn to assess for anemia as a result of hemorrhage or pernicious anemia. Diagnostic measures for detecting H. pylori infection. 11 Gastritis- Medical management Acute gastritis can be managed by: -Self repairing of gastric mucosa -Instructing the patient to refrain from alcohol and food until symptoms subside. -A nonirritating diet is recommended. -If the symptoms persist, (iv) fluids may needed. 12  Gastritis- Medical management If bleeding presents, management is supportive: -NG intubation -Antiacids, Histamine-2 receptor antagonists, PPI -IVF -Fiberoptic endoscopy -If extreme, surgery is indicated to remove the gangrenous or perforated tissue. 13 Gastritis- Medical management -A gastric resection or a gastrojejunostomy (anastomosis of jejunum to stomach to detour around the pylorus) may be necessary to treat gastric outlet obstruction, also called pyloric obstruction, a narrowing of the pyloric orifice, which cannot be relieved by medical management. -Chronic gastritis is managed by modifying the patient’s diet, promoting rest, reducing stress, recommending avoidance of alcohol and NSAIDs, and initiating medications that may include antibiotics, antacids, H2 blockers, or proton pump inhibitors, and antidiarrheal medications 14 (bismuthsalts)  15 Gastritis- Nursing Management: 1. Reducing anxiety 2. Promoting optional nutrition - Keep NPO - IVF - Later, introduce soft to solid foods gradually - Discourage the intake of caffeinated beverages, smoking, alcohol 16  Gastritis- Nursing Management: 3. Promoting fluid balance - Intake & output - Electrolytes - Any indicator of hemorrhagic gastritis (hematemesis) 4. Relieving pain 5. Promoting home, community-based and transitional care 17 Peptic Ulcer Disease Peptic ulcer may be referred to as a gastric, duodenal, or esophageal ulcer, depending on its location. A peptic ulcer is an excavation (hollowed-out area) that forms in the mucosa of the stomach, in the pylorus (the opening between the stomach and duodenum), in the duodenum or in the esophagus. 18  19 Peptic Ulcer Disease Erosion of mucosa is the cause. Then erosion may extends to muscle layers or through the muscle to the peritoneum (thin membrane that lines the inside of the wall of the abdomen) Peptic ulcers are more likely to occur in the duodenum than in the stomach. Chronic gastric ulcers tend to occur in the lesser curvature of the stomach, near the pylorus. Esophageal ulcers occur as a result of GERD. Men=women 20  Peptic Ulcer Disease Most peptic ulcers result from: -Infection with the gram-negative bacteria H. Pylori -The use of NSAIDs -Smoking and alcohol consumption. -Familial tendency -People with blood type O (higher HCL). -An association between peptic ulcer disease and COPD, liver cirrhosis, CRF, and autoimmune disorders. 21 Pathophysiology The erosion is caused by the increased concentration or activity of acid–pepsin or by decreased resistance of the normally protective mucosal barrier. A damaged mucosa cannot secrete enough mucus to act as a barrier against normal digestive juices. When the mucosal barrier is impaired, even normal or decreased levels of HCl may result in the formation of peptic ulcers 22  Pathophysiology Stress ulcer is the term given to the acute mucosal ulceration of the duodenal or gastric area that occurs after physiologically stressful events, such as burns, shock, sepsis, and multiple organ dysfunction syndrome. Stress ulcers are most common in patients who are ventilator-dependent after trauma or surgery. 23 Pathophysiology Curling ulcer is frequently observed about 72 hours after extensive burn injuries and often involves the antrum of the stomach or the duodenum. Cushing ulcer is common in patients with a traumatic head injury, stroke, brain tumor, or following intracranial surgery (stimulation of vagus nerve). Ulcers tend to be single and deep and may involve the esophagus, stomach, or duodenum 24  Clinical Manifestations Symptoms of peptic ulcer disease may last for a few days, weeks, or months and may disappear only to reappear, often without an identifiable cause. Many patients with peptic ulcers have no signs or symptoms: Silent peptic ulcer, (elderly, on aspirin and other NSAIDs) 25 Clinical Manifestations Patient with an ulcer (in general) complains of dull, gnawing ( a sensation of dull, constant) pain or a burning sensation in the midepigastrium or the back. Gastric ulcer: -Pain: immediately after eating -Onset: 30% to 40% of patients awake with pain during the night -Relieve of pain: less relieved with use of antacid Duodenal ulcer: -Pain: 2 to 3 hours after meals -Onset: 50% to 80% of patients awake with pain during the night -Relieve of pain: more likely to express relief of pain after eating or after taking an antacid 26  Clinical Manifestations Nonspecific symptoms: pyrosis, sour eructation (sour burp), vomiting, constipation or diarrhea, and bleeding. The patient with bleeding peptic ulcers: such as hematemesis (vomiting blood) or the passage of melena (black, tarry stools). Peptic ulcer perforation: severe, sharp upper abdominal pain, which may be referred to the shoulder; extreme abdominal tenderness; and nausea or vomiting. -Hypotension and tachycardia may occur, indicating the onset of shock 27 Assessment and Diagnostic Findings 1. A physical examination may reveal pain, epigastric tenderness, or abdominal distention. 2. Upper endoscopy, a biopsy of the gastric mucosa may be obtained 3. H. Pylori infection investigation: -Endoscopy and histologic examination. -Serologic testing for antibodies against the H. Pylori. -Stool antigen test -Urea breath test. 28  Assessment and Diagnostic Findings The patient who has a bleeding peptic ulcer may require periodic CBCs. Stools may be tested periodically until they are negative for occult blood. Gastric secretory studies (HCL level) 29 Medical Management 1. Pharmacologic Therapy: the most commonly used therapy for peptic ulcers is a combination of antibiotics, proton pump inhibitors, and sometimes bismuth salts that suppress or eradicate H. pylori. -The prescribed therapy id for 10-14 days, and may include triple therapy with two antibiotics (e.g., metronidazole [Flagyl] or amoxicillin [Amoxil] and clarithromycin plus a proton pump inhibitor (e.g., lansoprazole )or quadruple therapy with two antibiotics (metronidazole and tetracycline) plus a proton pump inhibitor and bismuth salts. -H2 blockers and proton pump inhibitors that reduce gastric acid secretion are used to treat ulcers not associated with H. pylori infection. 30  Medical Management The patient is advised to adhere and complete the medication regimen to ensure complete healing of the ulcer. The patient is advised to avoid the use of aspirin and other NSAIDs. Maintenance dosages of H2 blockers are usually recommended for 1 year. Patients at high risk for stress ulcers (e.g., patients who are mechanically ventilated for more than 48 hours) may be treated prophylactically 31 32  Medical Management 2.Smoking Cessation: Smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, resulting in increased acidity of the duodenum. 3. Dietary Modification: Diet modification to avoid over secretion of acid and hypermotility in the GI tract. Avoiding extremes of temperature in food and consumption of alcohol, coffee (decaffeinated coffee) Neutralize acid by eating three regular meals a day. 33 Medical Management 1. Surgical Management: Surgical procedures include vagotomy (transecting nerves that stimulate acid secretion) Antrectomy, which is removal of the pyloric (antrum) portion of the stomach with anastomosis (surgical connection) to either the duodenum (gastroduodenostomy or Billroth I) or jejunum (gastrojejunostomy or Billroth II). 34  35 Medical Management 1. Follow-Up Care: Recurrence of peptic ulcer disease within 1 year may be prevented with the prophylactic use of H2 blockers taken at a reduced dose. Patients who have had bleeding or gastric outlet obstruction, are at high a risk and requires a maintenance therapy. They should avoid smoking, coffee (including decaffeinated coffee) and other caffeinated beverages, alcohol, and ulcerogenic medications 36  The Patient with Peptic Ulcer Disease- NURSING DIAGNOSES Acute pain associated with the effect of gastric acid secretion on damaged tissue Interventions: -Administration of pain management -Avoid NSAIDs, aspirin -Avoid an alcohol -Meals should be eaten at regularly paced intervals -Relaxation techniques to help manage stress and pain 37 The Patient with Peptic Ulcer Disease- NURSING DIAGNOSES Anxiety associated with an acute illness Interventions: -The nurse assesses the patient’s level of anxiety -Explaining diagnostic tests -Administering medications as scheduled help reduce anxiety -The nurse interacts with the patient in a relaxed manner -Explains various coping techniques and relaxation methods -The patient’s family is also encouraged to participate in care and to provide emotional support. 38  The Patient with Peptic Ulcer Disease- NURSING DIAGNOSES Impaired nutritional intake associated with changes in diet Interventions: -Assesses the patient for malnutrition and weight loss -The patient is advised about the importance of adhering to the medication regimen and dietary restrictions. 39 Gastric Cancer The fifth most common cancer diagnosis A diet high in smoked, salted, or pickled foods and low in fruits and vegetables may increase the risk of gastric cancer H. Pylori infection is a major risk factor for the development of gastric cancer Gastritis, pernicious anemia, smoking, obesity, gastric ulcers The prognosis for patients with gastric cancer is generally poor The 5-year survival rate (32%) 40 Pathophysiology Ninety to 95% of gastric cancers are adenocarcinomas Gastric cancer begins with a lesion of the stomach mucosa. The lesion then penetrates cells in the deeper layers of the mucosa, submucosa, and stomach wall. 41 Clinical Manifestations Symptoms of early-stage disease may include pain that is relieved by antacids Symptoms of advanced disease are similar to those of peptic ulcer disease, such as dyspepsia, early satiety, weight loss, abdominal pain just above the umbilicus, loss or decrease in appetite, bloating after meals, and nausea or vomiting 42  Assessment and Diagnostic Findings The physical examination is usually not helpful Ascites and hepatomegaly (enlarged liver) may be apparent if the cancer cells have metastasized to the liver. Palpable nodules around the umbilicus Esophagogastroduodenoscopy for biopsy and cytologic washings is the diagnostic study of choice, and a barium x-ray examination of the upper GI tract Computed tomography (CT) A CBC may be used to evaluate for the presence of anemia 43 Medical Management 1. Surgical Management: -A total gastrectomy may be performed -A radical partial (subtotal) gastrectomy -Complications of gastric surgery: Dumping syndrome: within 10 to 30 minutes after a meal and often include early satiety, cramping abdominal pain, nausea, vomiting, and diarrhea. Hypoglycemia Bile reflux: burning epigastric pain that may increase after meals Gastric outlet obstruction 44  Medical Management 2. Chemotherapy and Targeted Therapy 3. Radiation Therapy 45 NURSING PROCESS-The Patient with Gastric Cancer 1. Anxiety associated with the disease and anticipated treatment 2. Impaired nutritional intake associated with early satiety or anorexia 3. Acute pain associated with tumor mass Grief associated with the diagnosis of cancer 4. Lack of knowledge regarding self-care activities 46 THANK YOU 47