Problems in Digestion MEDIUM

• Nutritional status relies on both intake and the function of the gastric and intestinal components of the GI system.
• Gastric and duodenal disorders are common, and nurses will encounter adults and older adults with these conditions across various clinical settings.

Gastritis

• Gastritis is the inflammation of the gastric or stomach mucosa.
• Approximately two million outpatient clinic visits are attributed to gastritis annually in the United States.
• It is increasingly prevalent in adults older than 60 years and affects women and men about equally.
• Gastritis can be acute (lasting hours to days) or chronic (resulting from repeated exposure to irritants).

Acute Gastritis

• Acute gastritis can be erosive or nonerosive, based on pathologic manifestations.
• Erosive acute gastritis is often caused by local irritants, like aspirin, NSAIDs, corticosteroids, alcohol, and gastric radiation therapy.
• Nonerosive acute gastritis is commonly caused by Helicobacter pylori (H. pylori) infection.
• H. pylori infects an estimated 50% of individuals globally.
• Severe acute gastritis may result from ingesting strong acids or alkalis, potentially leading to gangrene or perforation.
• Scarring from severe gastritis can cause pyloric stenosis or obstruction.
• Stress-related gastritis or ulcer can develop during acute illnesses, particularly after traumatic injuries, burns, severe infection, lack of stomach lining perfusion or major surgery.

Chronic Gastritis

• Classified by the underlying cause, often H. pylori infection.
• Chronic H. pylori gastritis is linked to peptic ulcers, gastric adenocarcinoma (cancer), and gastric mucosa-associated lymphoid tissue lymphoma.
• Chemical gastric injury (gastropathy) can result from long-term drug therapy (e.g., aspirin, NSAIDs) or duodenal content reflux after gastric surgery.
• Autoimmune disorders like Hashimoto thyroiditis, Addison disease, and Graves disease are associated with chronic gastritis.

Pathophysiology of Gastritis

• Gastritis involves disruption of the mucosal barrier protecting stomach tissue from digestive juices.
• Impaired barrier allows HCl, pepsin, and irritants (alcohol, NSAIDs, H. pylori) to contact the gastric mucosa, causing inflammation.
• Acute gastritis causes transient inflammation, leading to edema and hyperemia in the gastric mucosa, with superficial erosion.
• Superficial ulceration can occur due to erosive disease and may lead to hemorrhage.
• Chronic gastritis involves persistent inflammatory changes, eventually leading to atrophy (thinning) of gastric tissue.

Clinical Manifestations of Gastritis

• Acute gastritis symptoms include epigastric pain or discomfort, dyspepsia (indigestion), anorexia, hiccups, nausea, and vomiting, lasting hours to days.
• Erosive gastritis may cause bleeding, manifesting as blood in vomit or as melena (black, tarry stools) or hematochezia (bright red, bloody stools).
• Chronic gastritis symptoms include fatigue, pyrosis (heartburn) after eating, belching, sour taste, halitosis, early satiety, anorexia, nausea, and vomiting.
• Some patients with chronic gastritis may have mild epigastric discomfort or intolerance to spicy or fatty foods.
• Chronic gastritis can impair vitamin B12 absorption due to diminished intrinsic factor production, leading to pernicious anemia.

Assessment and Diagnostic Findings for Gastritis

• Definitive diagnosis involves endoscopy and histologic examination of a tissue specimen obtained by biopsy.
• A complete blood count (CBC) may be drawn to assess for anemia resulting from hemorrhage or pernicious anemia.
• Diagnostic measures are used for detecting H. pylori infection.

Medical Management of Gastritis

• Gastric mucosa can repair itself after acute gastritis; patients usually recover in about 1 day, with appetite returning in 2-3 days.
• Acute gastritis is managed by abstaining from alcohol and food until symptoms subside, followed by a nonirritating diet.
• Intravenous (IV) fluids may be needed if symptoms persist, and management is similar to upper GI tract hemorrhage control if bleeding is present.
• Supportive therapy includes nasogastric (NG) intubation, antacids, histamine-2 receptor antagonists (H2 blockers), proton pump inhibitors, and IV fluids.
• Fiberoptic endoscopy may be necessary, and in extreme cases, surgery may be required to remove gangrenous or perforated tissue.
• Gastric resection or gastrojejunostomy may be needed for gastric outlet obstruction (pyloric obstruction).
• Chronic gastritis is managed by modifying diet, promoting rest, reducing stress, avoiding alcohol and NSAIDs, and using antacids, H2 blockers, or proton pump inhibitors.
• H. pylori is often treated with a proton pump inhibitor, antibiotics, and sometimes bismuth salts.

Reducing Anxiety in Gastritis

• For patients who have ingested acids or alkalis, emergency measures may be necessary.
• Offer supportive therapy to the patient and family during treatment.
• Prepare the patient for additional diagnostic studies (endoscopies) or surgery.
• Use a calm approach to assess the patient and answer all questions as completely as possible.

Promoting Optimal Nutrition in Gastritis

• Provide physical and emotional support; help the patient manage nausea, vomiting, and pyrosis.
• The patient should take no foods or fluids by mouth until acute symptoms subside.
• Monitor fluid intake and output, along with serum electrolyte values, if IV therapy is necessary.
• Offer ice chips followed by clear liquids, then introduce solid food as soon as possible.
• Discourage intake of caffeinated beverages, alcohol, and cigarette smoking.
• Initiate and refer the patient for alcohol counseling and smoking cessation programs when appropriate.

Promoting Fluid Balance in Gastritis

• Monitor daily fluid intake and output to detect early signs of dehydration.
• If food and oral fluids are withheld, IV fluids (3 L/day) usually are prescribed.
• Maintain a record of fluid intake plus caloric value.
• Assess electrolyte values (sodium, potassium, chloride) every 24 hours to detect any imbalance.
• Be alert to indicators of hemorrhagic gastritis, which include hematemesis, tachycardia, and hypotension.
• Examine all stools for the presence of frank or occult bleeding.

Relieving Pain in Gastritis

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

Educating Patients About Self-Care for Gastritis

• Individualized education plans include information about stress management, diet, and medications.
• Dietary instructions should consider the patient’s daily caloric needs, cultural aspects of food preferences, and eating patterns.
• Review foods and other substances to be avoided (e.g., spicy, irritating, or highly seasoned foods; caffeine; nicotine; alcohol).
• Consultation with a dietitian may be recommended.
• Provide information about prescribed medications, which may include antacids, H2 blockers, or proton pump inhibitors; emphasize the importance of completing the H. pylori medication regimen.
• Provide information about lifelong vitamin B12 injections for patients with malabsorption.
• The nurse emphasizes the importance of keeping follow-up appointments with the primary provider.

Peptic Ulcer Disease

• Peptic ulcer disease affects approximately 4.6 million Americans annually, with peak onset between 30 and 60 years of age.
• A 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, pylorus, duodenum, or esophagus.
• Peptic ulcers are more likely to occur in the duodenum than in the stomach.
• Esophageal ulcers occur as a result of GERD.
• Women have an 8% to 11% and men have an 11% to 14% lifetime risk of developing peptic ulcers.

Factors Influencing Peptic Ulcer Development

• Rates of peptic ulcer disease among middle-age men have diminished, while rates among older adults have increased, particularly among women.
• Higher rates of NSAID use and H. pylori infections in older adult populations can explain this trend.
• Most peptic ulcers result from infection with H. pylori, which may be acquired through ingestion of food and water or person-to-person transmission.
• Predisposition depends on factors such as the type of H. pylori and other unknown factors.
• NSAIDs are a major risk factor, impairing the protective gastric mucosa and hindering GI tract repair.
• Smoking and alcohol consumption may be risks, familial tendency can also be a predisposing influence.
• People with blood type O are more susceptible, and there's an association with chronic obstructive pulmonary disease, cirrhosis, chronic kidney disease, and autoimmune disorders.

Zollinger-Ellison Syndrome (ZES)

• Rare condition with tumors in the pancreas and duodenum that secrete excessive gastrin.
• Excessive gastrin leads to extreme gastric hyperacidity and severe peptic ulcer disease.
• 25% to 30% of cases are linked to multiple endocrine neoplasia, type 1 (MEN-1).

Pathophysiology of Peptic Ulcers

• Peptic ulcers occur mainly in the gastroduodenal mucosa due to inability to withstand gastric acid (HCl) and pepsin.
• Erosion is caused by increased acid-pepsin or decreased resistance of the mucosal barrier.
• Damaged mucosa cannot secrete enough mucus to act as a barrier against digestive juices.
• Exposure to HCl, pepsin, NSAIDs, or H. pylori leads to inflammation, injury, and erosion.
• Duodenal ulcer patients secrete more acid, while gastric ulcer patients secrete normal or decreased levels.
• NSAIDs inhibit prostaglandin synthesis, disrupting the mucosal barrier, and damage results in decreased resistance to bacteria and H. pylori infection.

Pathophysiology of Zollinger-Ellison Syndrome

• Suspected when a patient has several peptic ulcers or an ulcer resistant to standard medical therapy.
• Identified by hypersecretion of gastrin, duodenal ulcers, and gastrinomas (islet cell tumors) in the pancreas or duodenum.
• More than 80% of gastrinomas are found in the "gastric triangle."
• Most gastrinomas grow slowly, however, more than 50% are malignant.
• Patients may experience epigastric pain, pyrosis, diarrhea, and steatorrhea (fatty stools).
• Associated with MEN-1 syndrome may have pituitary or parathyroid tumors.
• ZES-associated MEN-1 is diagnosed with hyperparathyroidism, which results in hypercalcemia for years before MEN-1 is diagnosed.

Stress Ulcers

• Acute mucosal ulceration in the duodenal or gastric area after stressful events.
• Common in patients following burn injuries, traumatic brain injury, or who require mechanical ventilation.
• Believed to be a result of ischemia to gastric mucosa and alterations in the mucosa barrier.
• Usually reversed when the patient recovers and caused by a disruption of the mucosal barrier and decreased mucosal blood flow (ischemia).
• Mucosal ischemia results in the reflux of duodenal contents into the stomach, which increases exposure of the unprotected gastric mucosa to the digestive effects of gastric acid (HCl) and pepsin.

Curling and Cushing Ulcers

• Curling ulcer is frequently observed 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.
• Cushing ulcer is caused by increased intracranial pressure, which results in overstimulation of the vagal nerve and an increased secretion of gastric acid (HCl).
• Cushing ulcers are typically deep, single ulcerations and have an increased risk of perforation.

Clinical Manifestations of Peptic Ulcers

• Symptoms may last for days, weeks, or months and may disappear, then reappear.
• Many patients have no signs or symptoms (silent peptic ulcers), commonly in older adults and those on aspirin or NSAIDs.
• Patients complain of dull, gnawing pain or a burning sensation in the mid epigastrium or the back.
• Gastric ulcer pain commonly occurs immediately after eating, whereas duodenal ulcer pain occurs 2 to 3 hours after meals.
• Patients with duodenal ulcers are more likely to express relief of pain after eating or after taking an antacid than patients with gastric ulcers.
• Other symptoms include pyrosis, vomiting, constipation or diarrhea, and bleeding, often accompanied by sour eructation (burping).

Assessment and Diagnostic Findings for Peptic Ulcers

• Physical examination may reveal pain, epigastric tenderness, or abdominal distention.
• Upper endoscopy is the preferred diagnostic procedure for direct visualization.
• Endoscopy allows biopsy of the gastric mucosa and suspicious lesions.
• H. pylori infection is determined by endoscopy and histologic examination of a tissue specimen obtained by biopsy, or a rapid urease test of the biopsy specimen.
• Less invasive diagnostic measures for detecting H. pylori include serologic testing for antibodies against the H. pylori antigen, stool antigen test, and urea breath test.
• Bleeding ulcers may require periodic CBCs to determine blood loss and the need for transfusions.
• Stools may be tested periodically until they are negative for occult blood.
• Gastric secretory studies are valuable in diagnosing ZES and achlorhydria, hypochlorhydria, or hyperchlorhydria.

Medical Management of Peptic Ulcers

• Once diagnosed, the patient should be informed about the possible management of the condition.
• Recurrence may develop; however, peptic ulcers treated with antibiotics to eradicate H. pylori have a lower recurrence rate than those that did not.
• Goals are to eradicate H. pylori and manage gastric acidity through medications, lifestyle changes, and surgical intervention.
• Combination drug therapy is the most common therapy for peptic ulcers and suppresses or eradicates H. pylori.
• Recommended combination drug therapy is typically prescribed for 10 to 14 days and may include triple therapy or quadruple therapy.
• H2 blockers and proton pump inhibitors reduce gastric acid secretion and treat ulcers not associated with H. pylori infection.
• Patients are advised to adhere to and complete the medication regimen and the use of NSAIDs should be avoided.
• Maintenance dosages of H2 blockers are usually recommended for 1 year.
• Hypersecretion of gastrin is controlled with proton pump inhibitors, for patients with ZES.
• Octreotide, a medication that suppresses gastrin levels, also may be prescribed.
• Patients with ZES will require periodic endoscopy to evaluate the effectiveness of medication therapy.
• Patients at high risk for stress ulcers may be treated prophylactically with either H2 blockers or proton pump inhibitors, and cytoprotective agents.

Smoking Cessation and Dietary Modification for Peptic Ulcers

• Smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, resulting in increased acidity and is associated with delayed healing of peptic ulcers.
• Intend to avoid oversecretion of acid and hypermotility in the GI tract through dietary modification.
• Extremes of temperature in food and beverages and overstimulation from consumption of alcohol, coffee, and caffeinated beverages should be avoided.
• Neutralize acid by eating three regular meals a day.
• The patient eats foods that are tolerated and avoids those that produce pain.

Surgical Management of Peptic Ulcers

• Surgery is usually recommended for patients with intractable ulcers, life-threatening hemorrhage, perforation, or obstruction and for those with ZES that is unresponsive to medications.
• Surgical procedures include vagotomy, with or without pyloroplasty, and antrectomy, which is removal of the pyloric (antrum) portion of the stomach with anastomosis to either the duodenum or jejunum.
• Surgeries may be performed through the use of laparoscopy and is determined by the surgeon’s preference and expertise, and the patient’s current health status; the presence of coexisting medical conditions; and a history of previous abdominal surgery.

Nursing Assessment for Peptic Ulcer Disease

• Ask the patient to describe the pain and its pattern.
• Determine how often emesis has occurred and note important characteristics of the vomitus.
• Ask the patient to list their usual food intake for a 72-h period.
• Lifestyle and other habits are a concern.
• Assess patient’s vital signs and reports of tachycardia and hypotension.

Nursing Interventions for Pain Relief in Peptic Ulcer Disease

• The patient should avoid NSAIDs, and alcohol.
• Eat meals at regularly paced intervals in a relaxed setting.
• Relaxation techniques should be learned to help manage stress and pain.

Nursing Interventions for Reduced Anxiety in Peptic Ulcer Disease

• The nurse assesses the patient’s level of anxiety.
• Explain diagnostic tests and administer medications as scheduled.
• Interact with the patient in a relaxed manner, help identify stressors, and explain coping techniques and relaxation methods.

Monitoring and Managing Potential Complications of Peptic Ulcers

   - Hemorrhage is a common cause of upper GI tract bleeding.

• Assess the patient for faintness or dizziness and nausea.
• Monitor vital signs frequently and evaluate the patient for tachycardia, hypotension, and tachypnea.
• Monitor hemoglobin and hematocrit, test the stool for gross or occult blood, and record hourly urinary output to detect anuria or oliguria.
• Patients suspected of having an ulcer who present with symptoms of acute GI bleeding should undergo evaluation with endoscopy.
• Administer saline lavage, suction decompression of gastric contents, and provide a means of monitoring further bleeding.

Perforation and Penetration

• Perforation is the erosion of the ulcer through the gastric serosa into the peritoneal cavity without warning and requires immediate surgery.
• Penetration is erosion of the ulcer through the gastric serosa into adjacent structures.
• Symptoms of penetration include back and epigastric pain not relieved by medications that were effective in the past, and requires surgical intervention.
• Signs and symptoms of perforation include the following:
  • Sudden, severe upper abdominal pain.
  • Vomiting.
  • Collapse.
  • Extremely tender and rigid abdomen.
  • Hypotension and Tachycardia.

Gastritis is the inflammation of the stomach mucosa, affecting millions in the US. It can be acute (erosive or nonerosive) or chronic, often linked to factors like NSAIDs, alcohol, or H. pylori. Nurses frequently encounter these conditions in various clinical settings.