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Management of Patients With Gastric and Duodenal Disorders Part 3

Management of Patients With Gastric and Duodenal Disorders Part 3. Miss Iman Shaweesh January 2008. An individual’s nutritional status depends not only on the type and amount of intake but also on the functioning of the gastric and intestinal portions of the gastrointestinal (GI) system.

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Management of Patients With Gastric and Duodenal Disorders Part 3

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  1. Management of PatientsWith Gastric andDuodenal DisordersPart 3 Miss Iman Shaweesh January 2008

  2. An individual’s nutritional status depends not only on the type and amount of intake but also on the functioning of the gastric and intestinal portions of the gastrointestinal (GI) system.

  3. Gastritis (inflammation of the gastric or stomach mucosa) is a common GI problem. 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. • Acute gastritis is often caused by dietary indiscretion—the person eats food that is contaminated with disease-causing microorganisms or that is irritating or too highly seasoned

  4. Gastritis • Other causes of acute gastritis include overuse of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), • excessive alcohol intake, bile reflux, and radiation therapy. • Severe form of acute gastritis is caused by the ingestion of strong acid or alkali, which may cause the mucosa to become gangrenous or to perforate.

  5. Gastritis • Chronic gastritis and prolonged inflammation of the stomach may be caused by either benign or malignant ulcers of the stomach or by the bacteria Helicobacter pylori. • Chronic gastritis is sometimes associated with autoimmune diseases such as pernicious anemia; dietary factors such as caffeine; the use of medications, especially NSAIDs; alcohol; smoking; or reflux of intestinal contents into the stomach.

  6. Pathophysiology • In gastritis, the gastric mucous membrane becomes edematous and hyperemic (congested with fluid and blood) and undergoes superficial erosion (Fig. 37-1). • It secretes a scanty amount of gastric juice, containing very little acid but much mucus. Superficial ulceration may occur and can lead to hemorrhage.

  7. Pathophysiology

  8. Clinical Manifestations • The patient with acute gastritis may have abdominal discomfort, headache, lassitude, nausea, anorexia, vomiting, and hiccupping. • Some have no symptoms. • The patient with chronic gastritis may complain of anorexia, heartburn after eating, belching, a sour taste in the mouth, or nausea and vomiting. Patients with chronic gastritis from vitamin deficiency usually have evidence of malabsorption of vitamin B12 caused by antibodies against intrinsic factor.

  9. Assessment and Diagnostic Findings • Gastritis is sometimes associated with hypochlorhydria (absence or low levels of hydrochloric acid [HCl]) or with hyperchlorhydria (high levels of HCl). • Diagnosis can be determined by endoscopy, upper GI radiographic studies, and histologic examination of a tissue specimen- biopsy. • diagnostic measures for detecting H. pylori include serologic testing for antibodies against the H. pylori antigen, and a breath test.

  10. Medical Management • The gastric mucosa is capable of repairing itself after a bout of gastritis. As a rule, the patient recovers in about 1 day. • nonirritating diet is recommended. • If bleeding is present, management is similar to the procedures used for upper GI tract hemorrhage • If itcaused by ingestion of strong acids or alkalis, treatment consists of diluting and neutralizing the offending agent. To neutralize acids, common antacids (eg, aluminum hydroxide)

  11. Medical Management • to neutralize an alkali, diluted lemon juice or diluted vinegar is used. • If corrosion is extensive or severe, emetics and lavage are avoided because of the danger of perforation and damage to the esophagus. Therapy is supportive and may include nasogastric (NG) intubation.analgesic agents and sedatives, antacids, and intravenous (IV) fluids. • Fiberoptic endoscopy may be necessary. In extreme cases, emergency surgery may be required to remove gangrenous or perforated tissue.

  12. Medical Management • Chronic gastritis is managed by modifying the patient’s diet, promoting rest, reducing stress, and initiating pharmacotherapy. • H. pylori may be treated with antibiotics (eg, tetracycline or amoxicillin, combined with clarithromycin) and a proton pump inhibitor (eg, lansoprazole [Prevacid]), and possibly bismuth salts (Pepto-Bismol) (Table 37-1). • Research is being conducted to develop a vaccine against H. pylori

  13. Histamine 2 (H2) Receptor Antagonists

  14. Proton (Gastric Acid) Pump Inhibitor

  15. Gastric and Duodenal Ulcers • A peptic ulcer is an excavation (hollowed-out area) that forms in the mucosal wall of the stomach, in the pylorus (opening between stomach and duodenum), in the duodenum (first part of small intestine), or in the esophagus. A peptic ulcer is frequently referred to as a gastric, duodenal, or esophageal ulcer, depending on its location, or as peptic ulcer disease.

  16. Peptic ulcers are more likely to be in the duodenum than in the stomach. As a rule they occur alone, but they may occur in multiples. Chronic gastric ulcers tend to occur in the lesser curvature of the stomach, near the pylorus. • In the past, stress and anxiety were thought to be causes of ulcers. Research has identified that peptic ulcers result from infection with the gram-negative bacteria H. pylori

  17. Familial tendency may be a significant predisposing factor. A further genetic link is noted in the finding that people with blood type O are more susceptible to peptic ulcers than are those with blood type A, B, or AB. There also is an association between duodenal ulcers and chronic pulmonary disease or chronic renal disease.

  18. Stress ulcers, which are clinically different from peptic ulcers, are ulcerations in the mucosa that can occur in the gastroduodenal area. Stress ulcers may occur in patients who are exposed to stressful conditions.

  19. DUODENAL ULCER Incidence Age 30–60 Male: female 2–3:1 80% of peptic ulcers are duodenal GASTRIC ULCER Usually 50 and over Male: female 1:1 15% of peptic ulcers are gastric Comparing Duodenal and Gastric Ulcers

  20. DUODENAL ULCER Hypersecretion of stomach acid (HCl) May have weight gain Pain occurs 2–3 hours after a meal; often awakened between 1–2 AM; ingestion of food relieves pain Vomiting uncommon GASTRIC ULCER Normal—hyposecretion of stomach acid (HCl) Weight loss may occur Pain occurs 1⁄2 to 1 hour after a meal; rarely occurs at night; may be relieved by vomiting; ingestion of food does not help, sometimes increases pain Vomiting common Signs, Symptoms, and Clinical Findings

  21. DUODENAL ULCER Hemorrhage less likely than with gastric ulcer, but if present melena more common than Hematemesis More likely to perforate than gastric ulcers GASTRIC ULCER Hemorrhage more likely to occur than with duodenal ulcer; hematemesis more common than melena Comparing Duodenal and Gastric Ulcers

  22. DUODENAL ULCER Malignancy Possibility Rare Risk Factors H. pylori, alcohol, smoking, cirrhosis, stress GASTRIC ULCER Occasionally H. pylori, gastritis, alcohol, smoking, use of NSAIDs, stress Comparing Duodenal and Gastric Ulcers

  23. Pathophysiology • Peptic ulcers occur mainly in the gastroduodenal mucosa because this tissue cannot withstand the digestive action of gastric acid (HCl) and pepsin. The erosion is caused by the increased concentration or activity of acid-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. Patients with duodenal ulcer disease secrete more acid than normal, whereas patients with gastric ulcer tend to secrete normal or decreased levels of acid.

  24. 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, severe sepsis, and multiple organ traumas. • Differences of opinion exist as to the actual cause of mucosal ulceration in stress ulcers. Usually, it is preceded by shock; this leads to decreased gastric mucosal blood flow and to reflux of duodenal contents into the stomach. In addition, large quantities of pepsin are released. The combination of ischemia, acid, and pepsin creates an ideal climate for ulceration.

  25. Pathophysiology • Stress ulcers should be distinguished from Cushing’s ulcers and Curling’s ulcers, two other types of gastric ulcers. • Cushing’s ulcers are common in patients with trauma to the brain. • Curling’s ulcer is frequently observed about 72 hours after extensive burns

  26. Clinical Manifestations • As a rule, the patient with an ulcer complains of dull, gnawing pain or a burning sensation in the midepigastrium or in the back. It is believed that the pain occurs when the increased acid content of the stomach and duodenum erodes the lesion and stimulates the exposed nerve endings. • pyrosis (heartburn), vomiting, constipation or diarrhea, and bleeding. Pyrosis is a burning sensation in the esophagus and stomach that moves up to the mouth. Heartburn is often accompanied by sour eructation, or burping, which is common when the patient’s stomach is empty. Fifteen percent of patients with gastric ulcers experience bleeding.

  27. Assessment and Diagnostic Findings • A physical examination may reveal pain, epigastric tenderness, or abdominal distention. • A barium study of the upper GI tract may show an ulcer; however, endoscopy is the preferred diagnostic procedure because it allows direct visualization of inflammatory changes, ulcers, and lesions-biopsy.

  28. Stools may be tested periodically until they are negative for occult blood. Gastric secretory studies are of value in diagnosing achlorhydria and ZES. H. pylori infection may be determined by biopsy and histology with culture. • There is also a breath test that detects H. pylori, as well as a serologic test for antibodies to the H. pylori antigen.

  29. Medical Management • peptic ulcers treated with antibiotics to eradicate H. pylori have a lower recurrence rate than those not treated with antibiotics. The goals are to eradicate H. pylori and to manage gastric acidity. Methods used include medications, lifestyle changes, and surgical intervention.

  30. PHARMACOLOGIC THERAPY • Currently, the most commonly used therapy in the treatment of ulcers is a combination of antibiotics, proton pump inhibitors, and bismuth salts that suppresses or eradicates H. pylori. • Rest, sedatives, and tranquilizers may add to the patient’s comfort and are prescribed as needed. Maintenance dosages of H2 receptor antagonists are usually recommended for 1 year.

  31. STRESS REDUCTION AND REST • SMOKING CESSATION • DIETARY MODIFICATION • SURGICAL MANAGEMENT • surgery is usually recommended for patients with intractable ulcers (those that fail to heal after 12 to 16 weeks of medical treatment), include vagotomy, with or without pyloroplasty, and the Billroth I and Billroth II procedures

  32. Severing of the vagus nerve. Decreases gastric acid by diminishing cholinergic stimulation to the parietal cells, making them less responsive to gastrin. May be done via open surgical approach, laparoscopy, or thoracoscopy

  33. A surgical procedure in which a longitudinal incision is made into the pylorus and transversely sutured closed to enlarge the outlet and relax the muscle

  34. Removal of the lower portion of the antrum of the stomach (which contains the cells that secrete gastrin) as well as a small portion of the duodenum and pylorus. The remaining segment is anastomosed to the duodenum (Billroth I) or to the jejunum (Billroth II)

  35. Removal of distal third of stomach; anastomosis with duodenum or jejunum. Removes gastrin-producing cells in the antrum and part of the parietal cells.

  36. Morbid Obesity • obesity is the term applied to people who are more than two times their ideal body weight or whose body mass index (BMI) exceeds 30 kg/m2. • Another definition of morbid obesity is body weight that is more than 100 pounds greater than the ideal body weigh. • Patients with morbid obesity are at higher risk for health complications, such as cardiovascular disease, arthritis, asthma, bronchitis, and diabetes. They frequently suffer from low self-esteem, impaired body image, and depression.

  37. Medical Management • There is a belief that depression may be a contributing factor to weight gain, and treatment of the depression with bupropion hydrochloride • Several medications have recently been approved for obesity. They include sibutramine HCl (Meridia) and orlistat (Xenical). By inhibiting the reuptake of serotonin and norepinephrine, sibutramine decreases appetite.

  38. Gastric bypass and vertical banded gastroplasty are the current operations of choice. These procedures may be performed laparoscopically or by an open surgical technique. In gastric bypass surgery, the proximal segment of the stomach is transected to form a small pouch with a small gastroenterostomy stoma. The Roux-en-Y gastric bypass is the recommended procedure for long-term weight loss. In this procedure, a horizontal row of staples creates a stomach pouch with a 1-cm stoma that is anastomosed with a portion of distal jejunum, creating a gastroenterostomy. The transected proximal portion of the jejunum is anastomosed to the distal jejunum.

  39. NSG Intervention • Complications that may occur in the immediate postoperative period include peritonitis, stomal obstruction, stomal ulcers, atelectasis and pneumonia, thromboembolism, and metabolic imbalances resulting from prolonged vomiting and diarrhea. • small feedings consisting of a total of 600 to 800 calories per day and encourages fluid intake to prevent dehydration.

  40. The nurse explains that noncompliance by eating too much or too fast or eating highcalorie liquid and soft foods results in vomiting and painful esophageal distention. The nurse discusses dietary instructions before discharge and schedules monthly outpatient visits.

  41. Gastric Cancer • Most of these deaths occur in people older than 40 years of age, but they occasionally occur in younger people. Men have a higher incidence of gastric cancers than women do. • Diet appears to be a significant factor. A diet high in smoked foods and low in fruits and vegetables may increase the risk of gastric cancer. • chronic inflammation of the stomach, pernicious anemia, achlorhydria, gastric ulcers, H. pylori infection, and genetics.

  42. Pathophysiology • Most gastric cancers are adenocarcinomas and can occur in any portion of the stomach. The tumor infiltrates the surrounding mucosa, penetrating the wall of the stomach and adjacent organs and structures. • Metastasis through lymph to the peritoneal cavity occurs later in the disease.

  43. Clinical Manifestations • Some studies show that early symptoms, such as pain relieved with antacids, resemble those of benign ulcers. • Symptoms of progressive disease may include anorexia, dyspepsia (indigestion), weight loss, abdominal pain, constipation, anemia, and nausea and vomiting.

  44. Assessment and Diagnostic Findings • physical examination is not helpful in detecting cancer because most gastric tumors are not palpable. Ascites may be apparent if the cancer cells have metastasized to the liver. • Endoscopy for biopsy and cytologic washings is the usual diagnostic study, and a barium x-ray examination of the upper GI tract may also be performed

  45. Because metastasis often occurs before warning signs develop, a computed tomography (CT) scan, bone scan, and liver scan are valuable in determining the extent of metastasis. • A complete x-ray examination of the GI tract should be performed when any person older than 40 years of age has had indigestion (dyspepsia) of more than 4 weeks’ duration.

  46. Medical Management • no successful treatment for gastric carcinoma except removal of the tumor. If the tumor can be removed while it is still localized to the stomach, the patient can be cured. • If the tumor has spread beyond the area that can be excised, cure is impossible. Palliative rather than radical surgery is performed if there is metastasis to other vital organs. • If a radical subtotal gastrectomy is performed, the stump of the stomach is anastomosed to the jejunum, as in the gastrectomy for ulcer.

  47. Chemotherapeutic medications include cisplatin, irinotecan, or a combination of 5-fluorouracil, doxorubicin (Adriamycin), and mitomycin-C. Some studies are being conducted on the use of chemotherapy before surgery. Radiation therapy also may be used for palliation. Assessment of tumor markers (blood analysis for antigens indicative of colon cancer) such as carcinoembryonic antigen, CA 19-9, and CA 50 may help determine the effectiveness of treatment.

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