Gastritis: Inflammation of the Gastric Mucosa

• Nutritional status relies on both intake and the function of the gastric and intestinal systems.
• Gastric and duodenal disorders are common, necessitating nursing care in various clinical settings

Gastritis

• Gastritis is the inflammation of the gastric or stomach mucosa.
• It leads to approximately two million outpatient clinic visits annually in the U.S.
• The prevalence of gastritis increases in adults older than 60 years.
• Men and women are equally affected by gastritis
• It may be acute (lasting hours to days) or chronic (resulting from repeated exposure to irritants).
• Acute gastritis is classified as erosive or nonerosive, based on pathologic manifestations.
• Erosive acute gastritis is caused by local irritants like aspirin, NSAIDs, corticosteroids, alcohol, and gastric radiation therapy
• Nonerosive acute gastritis is caused by infection with Helicobacter pylori (H. pylori), affecting around 50% of individuals globally
• Severe acute gastritis can result from ingesting strong acids or alkalis, leading to gangrene or perforation.
• Stress-related gastritis or ulcer can develop during acute illnesses, major traumatic injuries, burns, severe infection, lack of perfusion to the stomach lining, or major surgery.
• Chronic gastritis is classified by the underlying causative mechanism, often including H. pylori infection.
• Chronic H. pylori gastritis is implicated in peptic ulcers, gastric adenocarcinoma, and gastric mucosa–associated lymphoid tissue lymphoma.
• Chemical gastric injury from long-term drug therapy (aspirin, NSAIDs) or duodenal reflux after gastric surgery can cause chronic gastritis.
• Autoimmune disorders like Hashimoto thyroiditis, Addison disease, and Graves disease are associated with chronic gastritis

Pathophysiology

• Gastritis involves disruption of the mucosal barrier, which normally protects the stomach from digestive juices.
• HCl, pepsin, and other irritants come into contact with the gastric mucosa, resulting in inflammation.
• In acute gastritis, inflammation is usually transient, causing edema, hyperemia, and superficial erosion of the gastric mucosa.
• Superficial ulceration from erosive disease can lead to hemorrhage
• Persistent insults in chronic gastritis lead to chronic inflammatory changes and atrophy of gastric tissue.

Clinical Manifestations

• Rapid onset of epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting are symptoms of acute gastritis that can last from hours to days.
• Erosive gastritis may cause bleeding, manifesting as blood in vomit, melena, or hematochezia
• Chronic gastritis presents with fatigue, pyrosis after eating, belching, sour taste, halitosis, early satiety, anorexia, or nausea and vomiting.
• Some patients with chronic gastritis experience mild epigastric discomfort, intolerance to spicy or fatty foods, or pain relieved by eating.
• Vitamin B12 absorption may be impaired due to diminished intrinsic factor production, leading to pernicious anemia.

Assessment and Diagnostic Findings

• Endoscopy with histologic examination of a tissue specimen obtained by biopsy is used to diagnose gastritis.
• A complete blood count (CBC) may be drawn to assess anemia from hemorrhage or pernicious anemia.
• H. pylori infection diagnostic measures are discussed later in the Peptic Ulcer Disease section.

Medical Management

• The gastric mucosa can repair itself after acute gastritis.
• Patients typically recover in about 1 day, with diminished appetite for an additional 2 to 3 days
• Management includes avoiding alcohol and food until symptoms subside, followed by a nonirritating diet.
• IV fluids may be needed if symptoms persist
• Bleeding is managed similarly to upper GI tract hemorrhage, which is discussed later in this chapter.
• Therapy is supportive and includes nasogastric intubation, antacids, H2 blockers, proton pump inhibitors, and IV fluids.
• Fiberoptic endoscopy may be necessary
• Extreme cases may require emergency surgery to remove gangrenous or perforated tissue.
• Gastric resection or gastrojejunostomy may be needed for gastric outlet/pyloric obstruction that is not relieved by medical management.
• Chronic gastritis is managed through diet modification, rest, stress reduction, avoidance of alcohol and NSAIDs, and medications like antacids, H2 blockers, or PPIs.
• H. pylori may be treated with proton pump inhibitors, antibiotics, and sometimes bismuth salts

Nursing Management

Reducing Anxiety

• Emergency measures may be necessary if acids or alkalis have been ingested; supportive therapy is provided to the patient and family during and after treatment.
• Nurses should prepare patients for diagnostic studies (endoscopies) or surgery and calmly address their questions due to pain or planned treatment modalities.

Promoting Optimal Nutrition

• Provide support and management of nausea, vomiting, and pyrosis in acute gastritis.
• Patients should abstain from food or fluids until acute symptoms subside to allow the gastric mucosa to heal.
• Monitor fluid intake and output, along with serum electrolyte values, if IV therapy is necessary.
• Offer ice chips followed by clear liquids after symptoms subside, and introduce solid food as soon as possible.
• Discourage caffeinated beverages (increase gastric activity and pepsin secretion), alcohol, and cigarette smoking (increases gastric acid secretion and interferes with the mucosal barrier).
• Initiate referrals for alcohol counseling and smoking cessation programs when appropriate.
• Antibiotics (Amoxicillin, Clarithromycin, Metronidazole, and Tetracycline) are used to eradicate H. pylori bacteria in the gastric mucosa.
• Antidiarrheals (Bismuth subsalicylate) are used to suppress H. pylori bacteria in the gastric mucosa and assists with healing of mucosal ulcers.
• H2 Receptor Antagonists (Cimetidine, Famotidine, and Nizatidine) are used to decrease the amount of HCl produced by the stomach by blocking the action of histamine on histamine receptors of parietal cells in the stomach.
• Proton Pump Inhibitors of Gastric Acid (Esomeprazole, Lansoprazole, Omeprazole, Pantoprazole, and Rabeprazole) are used to decrease gastric acid secretion by slowing the H+, K+-ATPase pump on the surface of parietal cells.
• Prostaglandin E1 Analogue (Misoprostol) is a synthetic prostaglandin which protects the gastric mucosa from agents that cause ulcers and also increases mucus production and bicarbonate levels.
• Sucralfate creates a viscous substance in the presence of gastric acid which forms a protective barrier, binding to the surface of the ulcer, and prevents digestion by pepsin.

Promoting Fluid Balance

• Monitor daily fluid intake and output to detect dehydration (minimal fluid intake of 1.5 L/day, urine output of less than 1 mL/kg/h).
• Prescribe IV fluids if food and oral fluids are withheld (3 L/day) and maintain a record of fluid intake and caloric value.
• Assess electrolyte values every 24 hours to detect any imbalance.
• Be alert to indicators of hemorrhagic gastritis (hematemesis, tachycardia, hypotension) and examine stools for frank or occult bleeding.

Relieving Pain

• Instruct patients to avoid foods and beverages that irritate the gastric mucosa and use medications correctly to relieve chronic gastritis.
• Regularly assess the patient’s level of pain and the extent of comfort achieved through medication sand avoidance of irritating substances.

Promoting Home, Community-Based, and Transitional Care

• Evaluate the patient’s knowledge about gastritis and create an individualized stress management, diet, and medication education plan.
• Consider the patient’s daily caloric needs and cultural food preferences/patterns, and review foods and other substances to be avoided.
• Give information about prescribed medications (antacids, H2 blockers, or proton pump inhibitors).
• Reinforce the importance of completing the medication regimen for H. pylori eradication.
• Reinforce previous education and assess the patient’s symptoms and progress, vitamin B12 injections
• Emphasize the importance of keeping follow-up appointments with the primary care provider.

Peptic Ulcer Disease

• Peptic ulcer disease affects approximately 4.6 million Americans yearly with peak onset between 30 and 60 years.
• It involves an excavation (hollowed-out area) forming in the mucosa of the stomach, pylorus, duodenum, or esophagus.
• Erosion may reach the muscle layers or peritoneum.
• 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 happen as a result of GERD
• Women have an 8% to 11% and men have an 11% to 14% lifetime risk of developing peptic ulcers.
• Men in middle age ulcer rates have diminished over the past decades, with older adult rates increasing particularly among women.
• Those who are 65+ present to both outpatient and inpatient settings for treatment of peptic ulcers more than any other age group.
• This relates to higher occurrences of NSAID use and H. pylori infections in older adult populations
• Peptic ulcers are mainly from H. pylori infection, potentially acquired through food and water ingestion.
• Person-to-person transmission occurs through close contact and exposure to emesis
• NSAID use is a major risk factor for peptic ulcers
• Smoking and alcohol consumption may be risks, though the evidence is inconclusive
• People with blood type O are more susceptible to the development of peptic ulcers than are those with blood type A, B, or AB. -There is an association between peptic ulcer disease and chronic obstructive pulmonary disease, cirrhosis of the liver, chronic kidney disease, and autoimmune disorders.
• Zollinger-Ellison syndrome (ZES) is associated with peptic ulcer disease.
• ZES is the formation of benign or malignant tumors in the pancreas and duodenum that secrete excessive amounts of gastrin.
• 25% to 30% of ZES cases are liked to MEN-1 syndrome

Pathophysiology

• Peptic ulcers occur mainly in the gastroduodenal mucosa because it cannot withstand gastric acid (HCl) and pepsin.
• Erosion results from increased acid-pepsin concentration/activity or decreased mucosal barrier resistance.
• A damaged mucosa cannot secrete mucus as a barrier against digestive juices.
• Exposure leads to inflammation, injury, and erosion.
• Patients with duodenal ulcers secrete more acid, while those with gastric ulcers secrete normal/decreased acid levels.
• Impaired mucosal barriers can lead to peptic ulcers, even with normal acid levels
• NSAID use inhibits prostaglandin synthesis, disrupting the protective mucosal barrier and decreasing resistance to bacteria like H. pylori
• ZES is suspected in patients with multiple or treatment-resistant peptic ulcers.
• It is identified by hypersecretion of gastrin, duodenal ulcers, and gastrinomas in the pancreas or duodenum.
• Most gastrinomas are in the "gastric triangle" and tend to grow slowly, with more than 50% being malignant.
• Stress ulcers are acute mucosal ulcerations from burns, shock, sepsis, and multiple organ dysfunction syndrome.
• They are common in patients following significant burn injuries, TBI, or requiring mechanical ventilation and are a result of gastric mucosa ischemia and alterations in the mucosa barrier.
• Ulceration often comes from mucosal barrier disruption and decreased mucosal blood flow (ischemia).
• Mucosal ischemia leads to duodenal contents reflux into the stomach, increasing gastric mucosa exposure to HCl and pepsin, and creating an environment for ulceration

Clinical Manifestations

• Symptoms last days, weeks, or months and may recur without an identifiable cause.
• Many patients with peptic ulcers, especially older adults and NSAID users, have no signs or symptoms.
• The patient typically complains of dull, gnawing pain or a burning sensation in the mid epigastrium or the back.
• Gastric ulcer pain commonly occurs immediately after eating, while duodenal ulcer pain occurs 2 to 3 hours after meals.
• Other symptoms may include pyrosis, vomiting, constipation or diarrhea, and bleeding.
• Symptoms occur alongside sour eructation when the stomach is empty.
• Vomiting, can be caused from gastric outlet obstruction from pylorus spasms.
• Emesis contains undigested food eaten hours earlier.
• Constipation or diarrhea may occur due to diet and medications
• With bleeding peptic ulcers, patients may present with hematemesis or melena
• Peptic ulcer perforation results in sudden, severe upper abdominal pain, which may be referred to the shoulder.

Assessment and Diagnostic Findings

• A physical examination may reveal pain, epigastric tenderness, or abdominal distention.
• Upper endoscopy is the preferred diagnostic procedure for direct visualization of inflammatory changes, ulcers, and lesions.
• Biopsies can be performed.
• H. pylori infection can be determined by endoscopy, histologic examination of biopsy specimens, or rapid urease test.
• Other H. pylori diagnostic measures include serologic testing for antibodies, stool antigen test, and urea breath test.
• Patients with bleeding peptic ulcers may require periodic CBCs to determine blood loss and blood transfusion needs.
• Stools may be tested periodically until they are negative for occult blood.
• Gastric secretory studies are valuable in diagnosing ZES and achlorhydria

Medical Management

• Patients are informed that the condition can be managed.
• Eradicating H. pylori and managing gastric acidity are goals using medications, lifestyle changes, and surgical intervention
• Combination therapy with antibiotics, PPIs, and sometimes bismuth salts is commonly used to suppress or eradicate H. pylori. Bismuth subsalicylate, tetracycline, metronidazole and a PPI can be used for 10-14 days.
• H2 blockers and proton pump inhibitors reduce gastric acid secretion to treat ulcers not associated with H. pylori infection.
• Maintenance dosages of H2 blockers are usually recommended for 1 year.
• The hypersecretion of gastrin caused by ZES may be controlled with PPIs, with octreotide being prescribed to suppress gastrin levels.
• High-risk stress ulcer patients may receive prophylactic treatment with H2 blockers, PPIs, and cytoprotective agents.

Smoking Cessation

• Smoking decreases bicarbonate, increasing acidity of the duodenum
• Smoking delays peptic ulcer healing.

Dietary Modification

• Avoid Oversecretion of acid and hypermotility in the GI tract.
• Avoid extremes in food/beverage temperature and overstimulation from alcohol, caffeinated beverages
• Eating three regular meals a day helps to neutralize acid.
• Small, frequent feedings are not necessary if antacids or H2 blockers are taken.

Surgical Management

• Surgery is usually recommended for patients with intractable ulcers, life-threatening hemorrhage, perforation, or obstruction.
• It may be performed using a traditional open abdominal approach or through the use of laparoscopy.
• Follow-Up Care
• Recurrence may be prevented with long term use of H2 blockers.
• Likelihood of recurrence is reduced if the patient avoids smoking, and other caffeinated beverages, alcohol, and ulcerogenic medications

Nursing Process

Assessment

• The nurse asks the patient to describe the pain, its pattern and whether or not it occurs predictably as well as strategies used to relieve it. The nurse should also find out the patient vomit history.
• The nurses need to be aware of the lifestyle choices of the patient like smoking or ingesting alcohol.
• The nurse assesses the patient’s vital signs and reports tachycardia and hypotension, and also does a physical examination, including palpation of the abdomen for localized tenderness

Interventions

Relieving Pain

• achieved with prescribed medications and relaxation strategies.
• Patient should avoid NSAIDs and alcohol.
• Regularly paced meals in a relaxed setting help to reduce anxiety.

Reducing Anxiety

• Nurse should explain necessary testing that will be done and encourage the patient's family to participate.

Maintaining Optimal Nutritional Status

• The nurse assesses the patient for malnutrition and weight loss.

Complications to Monitor For

Hemorrhage

• Can be from acute or chronic gastritis
• Most common cause for upper GI bleeding
• Associated with 5% mortality rate
• Asses for faintness, dizziness, tachycardia and tachypnea.
• Interventions can include monitoring hemoglobin and hematocrit, testing the stool for gross or occult blood, and recording hourly urinary output.
• Manage hypotension using arteriography with embolization if needed.

Perforation

• Erosion of the ulcer through the gastric serosa into the peritoneal cavity.
• An abdominal emergency that requires immediate surgery.

Signs and symptoms include:

• Sudden, severe upper abdominal pain
• Vomiting
• Collapse
• Extremely tender and rigid abdomen
• Hypotension and tachycardia

Penetration

• Erosion of the ulcer through the gastric serosa into adjacent structures.
• Pain may be referred to the shoulders.

Gastritis is the inflammation of the stomach mucosa, affecting millions annually. It can be acute or chronic, with causes ranging from irritants like NSAIDs to H. pylori infection. Nursing care addresses both erosive and nonerosive forms.