Gastric and Duodenal Disorders

• Nutritional status is reliant on both intake and the function of the gastric and intestinal systems
• Gastric and duodenal disorders are common in the US, and nurses will encounter them across clinical settings

Key Terms Defined

• Achlorhydria: Absence of hydrochloric acid in gastric secretions.
• Antrectomy: Surgical removal of the stomach's pyloric section, connecting it to the duodenum (Billroth I) or jejunum (Billroth II).
• Dumping Syndrome: Rapid gastric emptying into the small intestine causing nausea, weakness, sweating, palpitations, syncope, and diarrhea.
• Duodenum: The initial segment of the small intestine
• Dyspepsia: Indigestion with upper abdominal discomfort related to eating.
• Gastric: Pertaining to the stomach.
• Gastric Outlet Obstruction: Mechanical blockage impeding normal gastric emptying.
• Gastritis: Stomach inflammation.
• Helicobacter Pylori (H. Pylori): Gram-negative bacterium colonizing the gastric mucosa, linked to peptic ulcer disease.
• Hematemesis: Vomiting blood.
• Hematochezia: Bright red, bloody stools.
• Melena: Black, tarry stools indicating occult blood.
• Omentum: Peritoneal fold surrounding the stomach and abdominal organs.
• Peritoneum: Membrane lining the abdominal wall and organs.
• Pyloroplasty: Surgery to widen the pyloric opening.
• Pylorus: The opening between the stomach and duodenum.
• Pyrosis: Heartburn.
• Serosa: Membrane covering the stomach's outer surface.
• Steatorrhea: Fatty, malodorous stools that float.
• Stenosis: Narrowing of a body passage.

Gastritis Overview

• Gastritis is the inflammation of the stomach mucosa
• It accounts for approximately two million outpatient clinic visits annually in the United States.
• Prevalence increases in adults over 60.
• It affects men and women about equally.
• Gastritis can be acute (lasting hours to days) or chronic (resulting from repeated exposure to irritants or recurring acute episodes).

Acute Gastritis Subtypes

• Acute gastritis is classified as erosive or nonerosive based on the gastric mucosa's pathologic findings
• Erosive gastritis is caused by local irritants like NSAIDs, corticosteroids, alcohol, and radiation therapy.
• Nonerosive gastritis is commonly caused by H. pylori infection

H. Pylori Infection

• 50% of individuals globally are infected with H. pylori
• Severe acute gastritis is caused by ingesting strong acids or alkalis
• This can lead to gangrene or perforation of the mucosa
• Scarring can cause pyloric stenosis or obstruction.
• Acute gastritis may result from severe trauma, burns, infection, or major surgery, referred to as stress-related gastritis or ulcer.

Chronic Gastritis

• Is classified by underlying cause, often H. pylori infection
• Chronic H. pylori gastritis is associated with peptic ulcers, gastric adenocarcinoma, and lymphoma.
• Chemical gastric injury from long-term drug use (NSAIDs) or duodenal reflux after gastric surgery can cause chronic gastritis.
• Autoimmune disorders like Hashimoto thyroiditis are linked to chronic gastritis.

Pathophysiology of Gastritis

• Gastritis involves the disruption of the stomach's protective mucosal barrier, leading to inflammation
• Inflammation is caused by corrosive HCl, pepsin, and irritants contacting the gastric mucosa.
• Acute gastritis causes edema, hyperemia, and superficial erosion of the gastric mucosa.
• Erosive disease can cause superficial ulceration and hemorrhage.
• Chronic gastritis leads to persistent inflammation and atrophy of gastric tissue.

Clinical Manifestations of Gastritis

• Acute gastritis presents with epigastric pain, dyspepsia, anorexia, hiccups, nausea, and vomiting lasting hours to days.
• Erosive gastritis can cause bleeding, showing as blood in vomit or melena or hematochezia.
• Chronic gastritis symptoms may include fatigue, pyrosis, belching, sour taste, halitosis, early satiety, anorexia, nausea, and vomiting.
• Chronic gastritis patients may experience mild epigastric discomfort or intolerance to spicy or fatty foods.
• Vitamin B12 absorption can be impaired in chronic gastritis due to decreased intrinsic factor production, potentially causing pernicious anemia.
• Some with chronic gastritis are asymptomatic.

Assessment and Diagnosis of Gastritis

• Endoscopy with biopsy is definitive for gastritis diagnosis
• CBC assesses anemia signs from hemorrhage or pernicious anemia.
• Diagnostic measures for detecting H. pylori are discussed later in the Peptic Ulcer Disease section.

Medical Management of Gastritis

• Acute gastritis typically resolves within a day
• Appetite may be reduced for a few additional days
• Management involves abstaining from alcohol and food until symptoms subside, followed by a nonirritating diet.
• Persistent symptoms require IV fluids.
• Bleeding is managed similarly to upper GI hemorrhage.
• Supportive therapy includes NG intubation, antacids, H2 blockers, proton pump inhibitors, and IV fluids.
• Endoscopy may be needed, and extreme cases may require surgery to remove gangrenous or perforated tissue.
• Gastric resection or gastrojejunostomy is used for gastric outlet obstruction.
• Chronic gastritis is managed by diet changes, rest, stress reduction, avoiding alcohol and NSAIDs, and medications like antacids, H2 blockers, or proton pump inhibitors.
• H. pylori is treated with proton pump inhibitors, antibiotics, and bismuth salts.

Nursing Management of Gastritis

• Offer supportive therapy to the patient and family
• Prepare them for diagnostic studies or surgery
• Use a calm approach to assess the patient and answer all questions
• The patient should not take food or fluids by mouth until the acute symptoms subside
• Monitor I/O's and serum electrolyte values
• Introduce solid food as soon as possible to provide adequate oral nutrition, decrease the need for IV therapy, and minimize irritation to the gastric mucosa
• Discourage intake of caffeinated beverages, alcohol use, and cigarette smoking
• Nicotine increases secretion of gastric acid and interfere with the mucosal barrier
• Initiate and refer the patient for alcohol counseling and smoking cessation programs

Pharmacologic Agents

• Antibiotics like Amoxicillin, Clarithromycin, Metronidazole, and Tetracycline
• Antidiarrheal like Bismuth subsalicylate
• H2 Receptor Antagonists like Cimetidine, Famotidine, and Nizatidine
• Proton Pump Inhibitors of Gastric Acid like Esomeprazole, Lansoprazole, Omeprazole, Pantoprazole, and Rabeprazole
• Prostaglandin El Analogue like Misoprostol
• Protectants like Sucralfate

Promoting Fluid Balance

• Daily fluid intake and output are monitored to detect early signs of dehydration (minimal fluid intake of 1.5 L/day, urine output of less than 1 mL/kg/h).
• If food and oral fluids are withheld, IV fluids (3 L/day) usually are prescribed and a record of fluid intake plus caloric value needs to be maintained.
• Electrolyte values are assessed every 24 hours to detect any imbalance
• All stools should be examined for the presence of frank or occult bleeding
• The primary provider should be notified, and the patient’s vital signs are monitored as the patient’s condition warrants
• Educate to avoid foods and beverages that may irritate the gastric mucosa as well as the correct use of medications

Promoting Home, Community-Based, and Transitional Care

• Educate patients about stress management, diet, and medications
• Dietary instructions emphasize daily caloric needs, cultural food preferences, and eating patterns
• Review foods and substances to avoid (e.g., spicy, irritating foods; caffeine; nicotine; alcohol).
• Completing the medication regimen as prescribed to eradicate H. pylori infection must be reinforced to the patient and caregiver
• Patients with malabsorption of vitamin B12 need information about lifelong vitamin B12 injections

Peptic Ulcer Disease (PUD)

• It affects approximately 4.6 million Americans annually, with the peak onset between 30 and 60 years of age
• A peptic ulcer is an excavation (hollowed-out area) that forms in the mucosa of the stomach, in the pylorus, in the duodenum or in the esophagus
• Erosion of a circumscribed area of mucosa is the cause
• 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 because of the backward flow of HCl from the stomach into the esophagus
• Rates among older adults have increased, particularly among women due to higher rates of NSAID use and H. pylori infections
• Research has documented that most peptic ulcers result from infection with H. pylori
• Transmission of the bacteria also occurs through close contact and exposure to emesis
• Both NSAIDs and H. pylori impair the protective gastric mucosa, and the failure of the GI tract to repair the mucosa may result in ulceration
• People with blood type O are more susceptible to the development of peptic ulcers
• Peptic ulcer disease is also associated with Zollinger-Ellison syndrome (ZES)

Pathophysiology of PUD

• Peptic ulcers occur in the gastroduodenal mucosa because this tissue cannot withstand the digestive action of gastric acid (HCl) and pepsin
• Erosion is caused by the increased concentration or activity of acid–pepsin or by decreased resistance of the normally protective mucosal barrier Exposure of the mucosa to gastric acid (HCl), pepsin, and other irritating agents leads to inflammation, injury, and subsequent erosion of the mucosa
• Patients with duodenal ulcers secrete more acid than normal, whereas patients with gastric ulcers tend to secrete normal or decreased levels of acid
• The use of NSAIDs inhibits prostaglandin synthesis, which is associated with a disruption of the normally protective mucosal barrier
• ZES is suspected when a patient has several peptic ulcers or an ulcer that is resistant to standard medical therapy
• 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
• Usually, the ulceration results from a disruption of the normally protective mucosal barrier and decreased mucosal blood flow (ischemia)
• 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 and is typically a deep single ulceration

Clinical Manifestations of PUD

• The patient with an ulcer complains of dull, gnawing pain or a burning sensation in the mid epigastrium or the back
• The pain associated with gastric ulcers most commonly occurs immediately after eating
• The pain associated with duodenal ulcers most commonly occurs 2 to 3 hours after meals
• Approximately 50% to 80% of patients with duodenal ulcers awake with pain during the night
• 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 nonspecific symptoms may include pyrosis, vomiting, constipation or diarrhea, and bleeding
• These symptoms are often accompanied by sour eructation (burping), which is common when the patient’s stomach is empty
• Vomiting may result from gastric outlet obstruction, which may contain undigested food eaten many hours earlier
• The patient with bleeding peptic ulcers may present with evidence of GI bleeding, such as hematemesis or the passage of melena
• The patient with peptic ulcer perforation often reports severe, sharp upper abdominal pain, which may be referred to the shoulder

Assessment and Diagnostic Findings of PUD

• A physical examination may reveal pain, epigastric tenderness, or abdominal distention
• Upper endoscopy is the preferred diagnostic procedure
• The patient who has a bleeding peptic ulcer may require periodic CBCs to determine the extent of blood loss
• Stools may be tested periodically until they are negative for occult blood
• Gastric secretory studies are of value in diagnosing ZES and achlorhydria, hypochlorhydria, or hyperchlorhydria.

Medical Management of PUD

• Once the diagnosis is established, the patient is informed that the condition can be managed
• The goals are to eradicate H. pylori as indicated and to manage gastric acidity
• Methods used include medications, lifestyle changes, and surgical intervention

Pharmacologic Therapy for PUD

• H2 blockers and proton pump inhibitors that reduce gastric acid secretion are used to treat ulcers not associated with H. pylori infection
• Smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, resulting in increased acidity of the duodenum
• Continued smoking is also associated with delayed healing of peptic ulcers
• The intent of dietary modification for patients with peptic ulcers is to avoid oversecretion of acid and hypermotility in the GI tract
• These can be minimized by avoiding extremes of temperature in food and beverages and overstimulation from the consumption of alcohol, coffee and other caffeinated beverages

Surgical Management of PUD

• 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

The Nursing Process for PUD

• The nurse asks the patient to describe the pain, its pattern and whether or not it occurs predictably in addition to strategies used to relieve it
• The nurse also asks the patient to list their usual food intake for a 72-h period and assesses lifestyle and other habits
• The nurse assesses the patient’s vital signs and reports tachycardia and hypotension, performs a physical examination including palpation of the abdomen for localized tenderness and tests stool for occult blood Potential complications include hemorrhage, perforation, penetration, and gastric outlet obstruction

Nursing Interventions for PUD

• Pain relief can be achieved with prescribed medications
• The patient should avoid NSAIDs, aspirin in particular, as well as alcohol
• Meals should be eaten at regularly paced intervals in a relaxed setting
• Medications prescribed to decrease gastric acid secretion are administered

Overview of gastric and duodenal disorders, common in the US, affecting nutritional status. Covers key terms like achlorhydria, antrectomy, dumping syndrome, and gastritis. Also addresses causes and treatments.