Management of Patients With Gastric and Duodenal Disorders PDF

Management of Patients With Gastric and Duodenal Disorders Dr. Magda Albeah  Management of patient with GIT disorders On completion of this chapter, the student will be able to: - Define key terms. - Compare the etiology, clinical manifestations, and management of acute gast...

Management of Patients With Gastric and Duodenal Disorders Dr. Magda Albeah  Management of patient with GIT disorders On completion of this chapter, the student will be able to: - Define key terms. - Compare the etiology, clinical manifestations, and management of acute gastritis, chronic gastritis, and peptic ulcer. - Use the nursing process as a framework for care of patients with gastritis and peptic ulcer. Function and anatomy of digestive system The primary digestive functions of the GI tract are the following:  To break down food particles into the molecular  To absorb into the bloodstream the small molecules produced by digestion  To eliminate undigested and unabsorbed foodstuffs and other waste products from the body Gastritis: Gastritis (inflammation of the gastric or stomach mucosa) is a common GI problem. Gastritis may be: Acute: Chronic:  lasting several hours to a  resulting from repeated few days, exposure to irritating agents or recurring episodes of acute gastritis  lasting several months  Pathophysiology:  Gastritis occurs as the result of a breakdown in the normal gastric mucosal barrier.  This mucosal barrier normally protects the stomach tissue from the corrosive action of HCl acid and pepsin.  When the barrier is broken, HCl acid and pepsin can diffuse back into the mucosa, this back diffusion results in tissue edema, disruption of capillary walls with loss of plasma into the gastric lumen, and possible hemorrhage. Gastritis: causes Acute gastritis caused by: Chronic gastritis caused by: contaminated food benign or malignant irritating food ulcers of the stomach too highly seasoned. bacteria : Helicobacter overuse of aspirin pylori. bile reflux, autoimmune diseases: radiation therapy pernicious anemia; ingestion of strong acid Caffeine; or alkali, Smoking; alcohol intake acute illnesses, as major traumatic injuries; burns; The use of medications such as NSAIDs Gastritis : Clinical Manifestations  Acute gastritis:  Chronic gastritis abdominal discomfort, anorexia, headache, lassitude, heartburn after eating, nausea, anorexia, vomiting, belching, a sour taste in Hiccupping the mouth, Epigastria tenderness and a nausea ,vomiting. feeling of fullness Vitamin deficiency Lasting from a few hours (malabsorption of to a few days, with vitamin B12) complete healing of the Lasting from a few mucosa expected. months to years Acute gastritis: Gastritis : The gastric mucosa is capable of repairing Medical Management itself: patient recovers in 1 day, appetite diminished for additional 2 Chronic gastritis : or 3 days.  Diet modification, After the patient can take nourishment by mouth,:  promoting rest, a non-irritating diet.  reducing stress, If symptoms persist, IV fluids given  initiating ingestion of strong acids or alkalis, diluting pharmacotherapy. and neutralizing the offending agent. Acids : antacids (eg, aluminum  Treated H. pylori hydroxide) may : an alkali: diluted lemon or vinegar antibiotics If corrosion is extensive, a proton pump emetics and lavage are avoided because of the danger of perforation inhibitor and damage to the esophagus. bismuth salts Assessment and diagnostic findings  - Endoscopy  - Upper GI radiographic studies  - Histologic examination of a tissue specimen obtained by biopsy  Nursing management - Daily fluid intake and output are monitored to detect early signs of dehydration (minimal urine output of 30 mL/hour, minimal intake of 1.5 L/day). - If food and fluids are withheld, IV fluids (3 L/day) usually are prescribed and a record of fluid intake plus caloric value (1 L of 5% dextrose in water = 170 calories of carbohydrate) needs to be maintained. - Electrolyte values (sodium, potassium, chloride) are assessed every 24 hours to detect imbalance.  The nurse must always be alert for any indicators of hemorrhagic gastritis, which include hematemesis (vomiting of blood), tachycardia, and hypotension  Peptic and duodenal ulcer At the end of this lecture, the student will be able to: - Define peptic and duodenal ulcer. - Explain types of ulcer. - Describe etiology and pathophysiology of ulcer. - Describe clinical manifestations of ulcer. - Identify diagnostic test of ulcer. - Management of patient with ulcer. - Use the nursing process as a framework for care of patients with peptic ulcer.  Education of patient with peptic ulcer.  Gastric and Duodenal Ulcers  A peptic ulcer is an excavation that forms in the mucosal wall of the stomach, in the: pylorus (opening between stomach and duodenum), duodenum (first part of small intestine), Or esophagus.  A peptic ulcer is referred either on its location as: gastric, duodenal, esophageal ulcer, or as peptic ulcer disease. Types of ulcer: 1. Peptic ulcers can be classified as acute or chronic, depending on the degree and duration of mucosal involvement, - The acute ulcer is associated with superficial erosion and minimal inflammation. It is of short duration and resolves quickly when the cause is identified and removed. Types of ulcer: -A chronic ulcer is one of long duration, eroding through the muscular wall with the formation of fibrous tissue. It is present continuously for many months or intermittently throughout the person’s lifetime.  Gastric or duodenal, according to the location.  Etiology and pathophysiology 1. Helicobacter pylori infection; the exact mechanism is unclear. 2. Non-steroidal anti-inflammatory drug (NSAID)–induced ulcers. Aspirin is the most ulcerogenic NSAID. 3. Hypersecretion of acid: Overactive vagus nerve, which stimulates the release of gastrin. (tea, coffee, cola, and chocolate) and smoking may also increase gastric acidity - Zollinger-Ellison syndrome: is tumors of the pancreas which increases secretion of gastrin (multiple peptic ulcers). Cont.  4. Genetic predisposition and stress.  5. People with blood type O.  6. Gastric tumors  Gastric and Duodenal Ulcers Pathophysiology The erosion is caused by increased concentration of decreased resistance of the or mucosa. acid-pepsin, Harmful Factor damaged mucosa cannot secrete enough mucus to act as a barrier against HCl Comparing Duodenal and Gastric Ulcers Duodenal Ulcer Gastric Ulcer  DUODENAL ULCER GASTRIC ULCER  Incidence  Incidence Age 30–60 Usually 50 and over Male: female 2:1 Male: female 1:1 Represent 80% of peptic ulcers Represent 15% of peptic ulcers  Signs, Symptoms,  Signs, Symptoms,  Lesion :Penetrating  Lesion :Superficial; smooth  HCl :Hyper secretion of (HCl) margins; round, oval or cone weight gain shaped Pain occurs 2–3 hours after  HCL :Normal—hyposecretion of (HCl a meal; ingestion of food relieves pain Weight loss Pain located to the right of the Pain occurs 1⁄2 to 1 hour after a midline epigastric region meal, ingestion of food doesn’t radiating to the back relieve pain, Describes as burning, - Pain occurring in the high left cramping, pressure like pain epigastric area radiating to the across midepigastrium & upper back & upper abdomen abdomen - Described as dull, aching, and gnawing,  DUODENAL ULCER GASTRIC ULCER Vomiting uncommon Vomiting common Hemorrhage less likely Hemorrhage more likely melena more common hematemesis more  Malignancy Possibility common Rare  Malignancy Possibility  Risk Factors Occasionally H. pylori, alcohol,  Risk Factors smoking, cirrhosis, H. pylori, gastritis, stress alcohol, smoking, use of NSAIDs, stress  Stress ulcer is the term given to the acute mucosal ulceration of the duodenal or gastric area that Stress ulcer occurs after physiologically Shock leads to : stressful events.  decreased gastric mucosal blood flow ( ischemia) burns, shock, severe sepsis,  reflux of duodenal contents multiple organ traumas. into the stomach (acid) ventilator-dependent patients  released large quantities of (pepsin). trauma surgery.  24 hours after injury: shallow erosions of the stomach wall; The combination of ischemia, acid, pepsin  72 hours: multiple gastric creates an ideal climate erosions are observed. for ulceration  When the patient recovers, the lesions are reversed.  Diagnostic evaluation of peptic ulcer  - Endoscopy is the preferred diagnostic procedure because it allows direct visualization of duodenal mucosa; inflammatory changes, ulcers, lesions, bleeding sites, and malignancy.  - Cytologic brushings and biopsies may be performed to obtained samples.  - Serial stool specimens to detect occult blood  - Gastric secretory studies (gastric acid secretion test and the serum gastric level test)— Gastric and Duodenal Ulcers Medical Management  H2 receptor antagonists, such as cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid) inhibits action of histamine on the H2 receptors of the parietal cells, thus reducing gastric acid output and concentration.  - Anti-secretory or proton pump inhibitor drug omeprazole (Prilosec) inhibits the production of hydrochloric acid in the stomach. Heals ulcers quickly (in 4 to 8 weeks). Gastric and Duodenal Ulcers Medical Management Cytoprotective drug sucralfate (Carafate) adheres to and protects the ulcer surface by forming a protective barrier against acid, bile, pepsin. Acid-neutralizing agents (antacids) provide additional relief of symptoms. Not used alone as treatment Antidiarrheal agent bismuth subsalicylate (Pepto-Bismol) has antibacterial action against H. pylori and enhances mucosal protection through bicarbonate and prostaglandin production. Antibiotics such as tetracycline and metronidazole (Flagyl) used with bismuth as ―triple therapy‖ to eradicate H. pylori. For NSAID ulcers discontinue NSAID and treat as mentioned above. Gastric and Duodenal Ulcers Medical Management  DIETARY MODIFICATION avoiding extremes of temperature and over- stimulation from consumption of:  meat extracts, alcohol,coffee)  caffeinated beverages,  diets rich in milk and cream (which stimulate acid secretion). neutralize acid by:  eating three regular meals a day.  Small, frequent feedings are not necessary as long as an antacid is taken. Diet compatibility ( individual matter):  eats foods that can be tolerated  And avoids those that produce pain. Gastric and Duodenal Ulcers Medical Management  SURGICAL MANAGEMENT surgery recommended for patients with:  intractable ulcers (those that fail to heal after 12 to 16 weeks of medical treatment),  life-threatening hemorrhage,  perforation,  obstruction, Gastric Surgery  peptic ulcers who have life-threatening:  gastric cancer  trauma.  Surgical procedures include: a vagotomy : (disconnecting nerves that stimulate acid secretion and opening the pylorus), pyloroplasty a partial gastrectomy, a total gastrectomy (removal of the stomach) esophagojejunal anastomosis  Gastric Surgery Pyloroplasty : Vagotomy : A surgical procedure in which a Decreases gastric acid by longitudinal incision is made diminishing cholinergic into the pylorus and transversely stimulation to the parietal cells, sutured closed making them less responsive to to enlarge the outlet and relax gastrin. May be done via open the muscle surgical approach,laparoscopy.  Gastric Surgery A. Billroth I Procedure: B. Billroth II Procedure: Removal of the lower portion of the Removal of distal third of stomach; antrum of the stomach (which contains Anastomosis with duodenum or jejunum. the cells that secrete gastrin) as Removes gastrin-producing cells in the well as a small portion of the duodenum antrum and part of the parietal cells. and pylorus.  Potential complications of peptic ulcer:  1. GI hemorrhage.  2. Ulcer perforation.  3. Pyloric obstruction (Gastric outlet obstruction).  Post-operative complications:  1. Dumping syndrome.  2. Postprandial hypoglycemia  Dumping syndrome  The term used for a group of unpleasant vasomotor and gastro intestinal symptoms include:  - Reducing the reservoir capacity of the stomach.  - Occur after gastric surgery in approximately one third to one half of patients. Cont.  - The stomach no longer has control over the amount of gastric chyme entering the small intestine.  - Consequently: A large bolus of a hypertonic fluid enters the intestine and result in fluid being drawn into the bowel lumen. This creates a decrease in plasma volume. Distension of the bowel lumen stimulates intestinal motility and the urge to defecate. Cont.  - The onset of symptoms occurs at the end of the meal or within 15-30 min after eating, lasts for no longer than an hour after meals.  - The patient usually describes: Feeling of generalized weakness, sweating, palpations, tachycardia, and dizziness. (These symptoms attributed to the sudden decreases in plasma volume), abdominal cramp, and the urge to defecate Postprandial hypoglycemia:  - As a bolus of fluid high in carbohydrate get into the small intestine results in hyperglycemia and the release of excessive amounts of insulin into the circulation.  - A secondary hypoglycemia then occurs 2 hours after meals. Cont.  - The immediate ingestion of sugared fluid or candy relieves the hypoglycemic symptoms.  - To avoid similar occurrence: the patient should be instructed to limit the amount of sugar consumed with each meal, and to eat small frequent meals with moderate amount of proteins and fat.  Nursing process for patient with ulcer:  Nursing assessment:  Determine location, character, and radiation of pain, factors aggravating or relieving pain, how long it lasts, when it occurs.  Ask about eating patterns, regularity, types of food, eating circumstances.  Take a social history of alcohol consumption and smoking.  Nursing process for patient with ulcer: Nursing assessment:  Ask about medications (especially aspirin, anti- inflammatory drugs, or steroids).  Determine if GI bleeding has been experienced.  Take vital signs, including lying, standing, and sitting blood pressures and pulses, to determine if orthostasis is present due to bleeding. Nursing diagnoses 1. Fluid volume deficit related to hemorrhage 2. Pain related to epigastric distress secondary to hypersecretion of acid, mucosal erosion, or perforation 3. Diarrhea related to GI bleeding or antacid therapy 4. Altered nutrition, less than body requirements, related to the disease process 5. Knowledge deficit related to physical, dietary, and pharmacologic treatment of disease Nursing interventions A. Avoiding fluid volume deficit  Monitor intake and output continuously to determine fluid volume status.  Observe stools for occult blood.  Monitor hemoglobin and hematocrit and electrolytes.  Administer prescribed IV fluids and blood replacement, as prescribed.  Insert an NG tube as prescribed and monitor the tube drainage for signs of visible and occult blood. B. Achieving pain relief: -Encourage bed rest to reduce physical activity and to separate patient from usual environment if pain continues. -Provide small, frequent meals to prevent gastric distention if not NPO. -Teach the patient that caffeine, alcoholic beverages, and nicotine may increase gastric acidity and promote erosion of the gastric mucosa. -Advise the patient about the irritating effects on the gastric mucosa of certain drugs, such as aspirin, NSAIDs, and certain antibiotics. -Administer prescribed medication  C. Decreasing diarrhea  Monitor patient’s elimination patterns to determine effects of medications.  Monitor vital signs and watch for signs of hypovolemia. Persistent diarrhea may be a sign of bleeding.  Restrict foods and fluids that promote diarrhea: raw vegetables, fruits, whole grain cereals, carbonated drinks.  Watch for signs of impaired skin integrity (erythema, soreness) around anus to promote comfort and decrease risk of infection. D. Achieving adequate nutrition:  Eliminate foods that cause pain.  Provide small, frequent feedings on time. This will decrease distention and the release of gastrin.  Advise the patient to avoid coffee and other caffeinated beverages as well as carbonated drinks; these may increase acid.  Advise the patient to avoid extremely hot or cold food or fluids, to chew thoroughly, and to eat in a leisurely fashion for better digestion.  Administer parenteral nutrition if bleeding is prolonged and patient is emaciated, as ordered. E. Educating about the following  Modify lifestyle to include health practices that will prevent recurrences of ulcer pain and bleeding.  Plan for rest periods and avoid or learn to cope with stressful situations; avoid fatigue.  Avoid specific foods known to cause the individual patient distress and pain.  Recognize signs of potential problems (mid epigastric pain). Reinstitute anti-ulcer medication if necessary.  - Take antacids 1 hour after meals, at bedtime, and when needed. Feed back A 35-year-old female is admitted for a medical unit. During physical examination she explain to the examiner the character of epigastric pain , all of the following risk factors are elicited. Which one is most likely to have contributed to the development of duodenal ulcer? Moderate  a. She usually slows a bowel movement.  b. She have a chronic ulcer from long durations  c. Hyper secretion of gastric acid  d. She usually complain from weight loss q2 A 55-year-old female is admitted to the hospital. During the nursing assessment, all of the following risk factors are elicited. Which one is most likely to have contributed to the chronic gastritis? Moderate  a. The patient has had four pregnancies.  b. The patient eats bran every day.  c. The patient has Helicobacter pylori  d. The patient had a metabolic problem q3 An adult patient is being treated for a peptic ulcer. The physician has prescribed H2 receptor antagonists as ranitidine or (Zantac) for which reason? High  a. Thus to reducing gastric acid output and concentration  b. It coats the gastric mucosa with a protective membrane.  c. It increases the sensitivity of histamine (H2) receptors.  d. It neutralizes acid in the stomach.  q4 An female patient is being treated for a stress ulcer. The physician has prescribed Omeprazole as a proton pump inhibitor drug for which from the following reason? High  a. Inhibits the production of hydrochloric acid in stomach.  b. It coats the gastric mucosa with a protective membrane.  c. It decreased the sensitivity of histamine (H2) receptors.  d. It neutralizes acid in the gastric area. q5  An adult patient is being treated form gastric ulcer. The physician has prescribed Cytoprotective drug sucralfate for which from the following reason? High  a. Adheres to and protects the ulcer surface by forming a protective barrier against acid, bile, pepsin  b. To inhibits the production of hydrochloric acid in the stomach.  c. It coats the gastric mucosa with a protective membrane.  d. It decreased the sensitivity of histamine (H2) Q6 and q7  Which one of the following is the predisposing factor for duodenal ulcers? Low  a. Eating spicy foods. b. A stressful life.  c. Hyper secretion of acid. d. Excessive caffeine intake.  Which of the following is the priority nursing diagnosis for a patient with massive peptic ulcers disease? Low  a. Fluid volume deficit related to hemorrhage  b. Deficient knowledge related to lack of information.  c. Acute pain related to epigastric erosion and acid buildup.  d. Ineffective coping related to diagnosis of peptic ulcers. End lecture In class activity: Case Study: Clinical summary:  Medical diagnosis: Peptic Ulcer  45-year-old female admitted with a 5 month history of persistent abdominal pain, vomiting for several days and blood with stool, which lead patient to seek for medical help. On admission, her vital signs were stable: temperature, 37.9°C ; O2 saturation ranging from 90-92 without O2 therapy and 95-98 with O2 therapy  Physical assessment Finding: shortness of breath Productive cough Breathe sound show wheezing heard all over the lung The patient said she is having moderate abdominal pain Patient is having abdominal distention and constipation since one week  laboratory values included: white blood cell count, 11,6 (normal: (4-11) 10.e12/l hemoglobin level, 8 g/dL (normal, 13 to 18);  Medication include: omeprazole 40 mg PO ,BID Folic acid 5mg PO OID atrovent 250 mg inhhal Q6H Continues O2 4l/hr lactulose 30 CC PO OID  In effective air way clearance; wheezing Impaired gas Secretion Productive cough Altered nutrition; exchange; atrovent 250 mg Hb; 8 g/l O2 saturation = 92% Peptic ulcer Hb; 8 g/l Folic acid, O2 2l/hr ferrous sulphate Reason for seeking constipation medical health; Anemia Constipation; Abdominal pain pain; 7 days no stool Vomiting Peptic ulcer Abdominal distension Patient complain Blood in stool Lactulose 30 cc Omeprazole 40 mg Infection; Temp. 37.9 WBC;11.6  Nursing diagnosis: objectives Ineffective air way clearance related to To maintain a patent accumulation of secretion air way Impaired gas Exchange related to To improve gas perfusion abnormalities exchange Altered nutrition less than body To maintain adequate requirement related to food nutrition intolerance. abdominal pain related to the effect of To relieve pain gastric acid secretion on damaged tissue Constipation related to disease process To maintain bowel movement infection related to pulmonary To prevent infection secretion