Problems in Digestion EASY

• Achlorhydria means a lack of hydrochloric acid in the stomach's digestive secretions.
• Antrectomy involves removing the pyloric (antrum) part of the stomach and surgically connecting it to either the duodenum (gastroduodenostomy/Billroth I) or the jejunum (gastrojejunostomy/Billroth II).
• Dumping syndrome is a physiologic response to rapid emptying of stomach contents into the small intestine, causing symptoms like nausea, weakness, sweating, palpitations, syncope, and diarrhea (also known as vagotomy syndrome).
• The duodenum is the first part of the small intestine, located between the stomach and jejunum.
• Dyspepsia means indigestion or upper abdominal discomfort related to eating.
• Gastric refers to the stomach.
• Gastric outlet obstruction is a condition where the pylorus and duodenum channel is mechanically blocked, preventing normal stomach emptying (also called pyloric obstruction).
• Gastritis is inflammation of the stomach.
• Helicobacter pylori (H. pylori) is a spiral-shaped, gram-negative bacterium colonizing the gastric mucosa and is involved in most cases of peptic ulcer disease.
• Hematemesis is vomiting blood.
• Hematochezia is bright red, bloody stools.
• Melena is tarry or black stools, indicating occult blood.
• Omentum is a fold of the peritoneum surrounding the stomach and other abdominal organs.
• Peritoneum is the thin membrane lining the abdominal wall and covering abdominal organs.
• Pyloroplasty is a surgical procedure to widen the pyloric orifice.
• The pylorus is the opening between the stomach and duodenum.
• Pyrosis is a burning sensation in the stomach and esophagus that moves up to the mouth (also known as heartburn).
• Serosa is the thin membrane covering the outer stomach surface; the visceral peritoneum.
• Steatorrhea is fatty stool, typically malodorous with oily appearance and floats in water.
• Stenosis is narrowing or tightening of a body opening or passage.
• Nutritional status depends on food intake and the function of the gastric and intestinal parts of the GI system.
• Nurses encounter adults with gastric and duodenal disorders frequently in inpatient and outpatient settings.

Gastritis

• Gastritis, or inflammation of the stomach lining, affects many Americans, especially adults over 60.
• It affects men and women equally.
• Gastritis can 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 present in the gastric mucosa.
• The erosive form is caused by irritants like aspirin, NSAIDs, corticosteroids, alcohol, and radiation therapy.
• The nonerosive form is caused by H. pylori infection, which affects approximately 50% of individuals globally.
• Severe acute gastritis can result from ingesting strong acids or alkalis, potentially leading to gangrene, perforation, pyloric stenosis, or obstruction.
• Acute gastritis can also occur due to major injuries, burns, severe infection, lack of perfusion to the stomach lining, or major surgery (stress-related gastritis or ulcer).
• Chronic gastritis is often linked to H. pylori infection and can lead to peptic ulcers, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma.
• Other causes of chronic gastritis include chemical gastric injury from long-term drug use (aspirin, NSAIDs) or duodenal reflux after gastric surgery, and autoimmune disorders like Hashimoto thyroiditis, Addison disease, and Graves disease.

Pathophysiology of Gastritis

• Gastritis involves a disruption of the mucosal barrier, which normally protects the stomach from digestive juices.
• Impairment of the barrier allows corrosive HCl, pepsin, and other irritants to inflame the gastric mucosa.
• In acute cases, inflammation is transient, causing edema, hyperemia, and superficial erosion.
• Superficial ulceration and hemorrhage may occur.
• Chronic gastritis leads to persistent inflammation and atrophy of gastric tissue.

Clinical Manifestations

• Acute gastritis symptoms include epigastric pain/discomfort, dyspepsia, anorexia, hiccups, nausea, and vomiting, lasting hours to days.
• Erosive gastritis can cause bleeding, manifesting as blood in vomit, melena, or hematochezia.
• Chronic gastritis symptoms include fatigue, pyrosis after eating, belching, sour taste, halitosis, early satiety, anorexia, and nausea/vomiting.
• Some individuals may experience mild epigastric discomfort or intolerance to spicy/fatty foods, relieved by eating.
• Chronic gastritis can lead to vitamin B12 malabsorption due to reduced intrinsic factor production, potentially causing pernicious anemia.

Assessment and Diagnostic Findings

• Diagnosis involves endoscopy and tissue biopsy.
• A complete blood count (CBC) assesses for anemia.
• Diagnostic measures detect H. pylori infection.

Medical Management

• The gastric mucosa can repair itself after acute gastritis, with recovery in approximately 1 day, although appetite may be diminished for a few days.
• Management of acute gastritis includes abstaining from alcohol and food until symptoms subside, followed by a nonirritating diet.
• Intravenous fluids may be necessary for persistent symptoms. Bleeding is managed like upper GI tract hemorrhage.
• Supportive therapy includes nasogastric (NG) intubation, antacids, H2 blockers, proton pump inhibitors, and IV fluids.
• Fiberoptic endoscopy may be required. In extreme cases, surgery removes gangrenous or perforated tissue.
• Gastric resection or gastrojejunostomy treat gastric outlet obstruction, a narrowing of the pyloric orifice.
• Chronic gastritis is managed via diet modification, rest, stress reduction, alcohol/NSAID avoidance, and medications (antacids, H2 blockers, proton pump inhibitors).
• H. pylori is treated with drug combinations: proton pump inhibitor, antibiotics, and sometimes bismuth salts.

Nursing Management

• The nurse offers supportive therapy to the patient and family during treatment and after the ingested acid or alkali has been neutralized or diluted.
• For acute gastritis, withhold oral foods/fluids until symptoms subside.
• Provide ice chips and clear liquids as symptoms improve, then introduce solids.
• Monitor fluid intake/output and electrolyte values.
• Discourage caffeinated beverages, alcohol, and smoking.
• Initiate alcohol counseling and smoking cessation programs.
• Monitor daily fluid intake and output. IV fluids are usually prescribed (3 L/day).
• Electrolyte values (sodium, potassium, chloride) are assessed every 24 hours to detect any imbalance.
• Monitor for hemorrhagic gastritis, indicated by hematemesis, tachycardia, and hypotension.
• Examine stools for frank or occult bleeding.

Relieving Pain

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

Promoting Home, Community-Based, and Transitional Care

Educating Patients About Self-Care

• Develop an individualized education plan that includes information about stress management, diet, and medications
• Dietary instructions take into account the patient’s daily caloric needs as well as cultural aspects of food preferences and patterns of eating.
• Provide information about prescribed medications, which may include antacids, H2 blockers, or proton pump inhibitors.

Continuing and Transitional Care

• Reinforce previous education and conduct ongoing assessment of the patient’s symptoms and progress.
• Patients with malabsorption of vitamin B12 need information about lifelong vitamin B12 injections; the nurse may instruct a family member or caregiver how to administer the injections or make arrangements for the patient to receive the injections from the primary provider.
• Emphasize 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 the peak onset between 30 and 60 years of age.
• A peptic ulcer may be gastric, duodenal, or esophageal.
• A peptic ulcer is an excavation (hollowed-out area) in the mucosa of the stomach, pylorus, duodenum, or esophagus.
• Erosion may reach muscle layers or the peritoneum.
• Peptic ulcers are more common in the duodenum than in the stomach.
• Chronic gastric ulcers often occur on the lesser curvature near the pylorus.
• Esophageal ulcers result from HCl backflow from the stomach (GERD).
• The rates of peptic ulcer disease among middle-age men have diminished over the past several decades, whereas the rates among older adults have increased, particularly among women.
• Stress and anxiety were previously linked to peptic ulcers, but research indicates that most peptic ulcers result from infection with H. pylori, which may be acquired through ingestion of food and water. Person-to-person transmission of the bacteria also occurs through close contact and exposure to emesis. .
• It is not known why H. pylori infection does not cause ulcers in all people, but most likely the predisposition to ulcer formation depends on certain factors, such as the type of H. pylori and other as yet unknown factors
• NSAID use is a major risk factor for peptic ulcers because it impairs gastric mucosa protection and repair. Smoking and alcohol may be risks, but 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 also is an association between peptic ulcer disease and chronic obstructive pulmonary disease, cirrhosis of the liver, chronic kidney disease, and autoimmune disorders.
• ZES is a condition with benign/malignant tumors in the pancreas and duodenum secreting excessive gastrin.
• This extreme hyperacidity leads to severe peptic ulcer disease.
• 25–30% of ZES cases are linked to multiple endocrine neoplasia, type 1 (MEN-1).

Pathophysiology

• Peptic ulcers mainly occur in the gastroduodenal mucosa due to its inability to withstand gastric acid (HCl) and pepsin.
• Erosion arises from increased acid-pepsin activity or decreased mucosal barrier resistance.
• A damaged mucosa lacks sufficient mucus secretion to protect against digestive juices.
• Exposure to gastric acid (HCl), pepsin, NSAIDs, or H. pylori causes inflammation, injury, and erosion.
• Duodenal ulcer patients secrete more acid than normal; gastric ulcer patients secrete normal/decreased acid.
• Impaired mucosal barriers, even with normal/decreased HCl, can lead to peptic ulcers.
• NSAIDs inhibit prostaglandin synthesis, disrupting the protective mucosal barrier.
• Damage to the barrier reduces resistance to bacteria, enabling H. pylori infection.
• ZES is indicated by hypersecretion of gastrin, duodenal ulcers, and gastrinomas (islet cell tumors).
• More than 80% of gastrinomas are in the "gastric triangle."
• Most gastrinomas grow slowly, but over 50% are malignant.
• ZES patients may experience epigastric pain, pyrosis, diarrhea, and steatorrhea.
• ZES-associated MEN-1 syndrome is diagnosed with hyperparathyroidism; therefore, patients may exhibit signs of hypercalcemia for several years before MEN-1 is diagnosed.
• Stress ulcers 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.
• Stress ulcers are believed to be a result of ischemia to gastric mucosa and alterations in the mucosa barrier.
• Curling ulcers are observed after extensive burn injuries and involve the antrum or duodenum.
• Cushing ulcers are common in patients with traumatic head injuries, stroke, brain tumors, or intracranial surgery.
• Cushing ulcers are thought to be caused by increased intracranial pressure, which results in overstimulation of the vagal nerve and an increased secretion of gastric acid (HCl).

Clinical Manifestations

• Peptic ulcer symptoms may last days, weeks, or months, and may disappear only to reappear, often without an identifiable cause.
• Many patients with peptic ulcers have no signs or symptoms. These silent peptic ulcers most commonly occur in older adults and those taking aspirin and other NSAIDs.
• Usually, patients experience a dull, gnawing or burning sensation in the mid-epigastrium or back.
• Gastric ulcer pain occurs immediately after eating, whereas duodenal ulcer pain occurs 2 to 3 hours after meals.
• Approximately 50% to 80% of patients with duodenal ulcers awake with pain during the night, whereas 30% to 40% of patients with gastric ulcers voice this type of complaint.
• Patients with duodenal ulcers report pain relief after eating or taking antacids, unlike gastric ulcer patients.
• Other symptoms include pyrosis, vomiting, constipation/diarrhea, and bleeding, accompanied by burping when the stomach is empty.
• Vomiting may result from gastric outlet obstruction due to pylorus spasms or mechanical obstruction.
• The emesis 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.
• Peptic ulcer perforation causes sudden, sharp upper abdominal pain referred to the shoulder, extreme tenderness, and nausea/vomiting, and hypotension and tachycardia may occur, indicating the onset of shock

Assessment and Diagnostic Findings

• Physical examination may reveal pain, epigastric tenderness, or abdominal distention.
• Upper endoscopy allows visualization of inflammatory changes, ulcers, and lesions.
• Endoscopy can obtain biopsies for histologic examination to check for H. pylori.
• Less invasive H. pylori tests include serologic testing, stool antigen test, and urea breath test.
• Bleeding peptic ulcer patients may need periodic CBCs to assess blood loss.
• Stools are tested until negative for occult blood.
• Gastric secretory studies diagnose ZES, achlorhydria, hypochlorhydria, or hyperchlorhydria.

Medical Management

• The patient is informed that the condition can be managed.
• Recurrence may develop; however, 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 as indicated and to manage gastric acidity.

Pharmacologic Therapy

• Therapy for peptic ulcers is a combination of antibiotics, proton pump inhibitors, and sometimes bismuth salts that suppress or eradicate H. pylori.
• Recommended combination drug therapy is prescribed for 10 to 14 days and may include triple therapy with two antibiotics plus a proton pump inhibitor or quadruple therapy with two antibiotics plus a proton pump inhibitor and bismuth salts
• H2 blockers and proton pump inhibitors that reduce gastric acid secretion are used to treat ulcers not associated with H. pylori infection.
• The patient is advised to adhere to and complete the medication regimen to ensure
• complete healing of the ulcer. The patient also is advised to avoid the use of NSAIDs.
• Maintenance dosages of H2 blockers are usually recommended for 1 year.
• Octreotide, a medication that suppresses gastrin levels, also may be prescribed (Daniels, Khalili, Morano, et al., 2019).
• Patients at high risk for stress ulcers may be treated prophylactically with either H2 blockers or proton pump inhibitors, and cytoprotective agents because of the increased risk of upper GI tract hemorrhage.

Smoking Cessation

• Smoking decreases bicarbonate secretion into the duodenum.
• Continued smoking is associated with delayed ulcer healing.

Dietary Modification

• 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 coffee and other caffeinated beverages and alcohol.
• In addition, an effort is made to neutralize acid by eating three regular meals a day.
• The patient eats foods that are tolerated and avoids those that produce pain.

Surgical Management

• Surgery is usually recommended for patients with intractable ulcers, life-threatening hemorrhage, perforation, or obstruction.
• Surgical procedures include vagotomy, with or without pyloroplasty and antrectomy, which is removal of the pyloric (antrum) portion of the stomach with anastomosis (surgical connection) to either the duodenum or jejunum.
• Surgery may be performed using a traditional open abdominal approach or through the use of laparoscopy.

Follow-Up Care

• Recurrence of peptic ulcer disease within 1 year may be prevented with the prophylactic use of H2 blockers taken at a reduced dose.
• The likelihood of recurrence is reduced if the patient avoids smoking, coffee and other caffeinated beverages, alcohol, and ulcerogenic medications (e.g., NSAIDs).

Nursing Process: Assessment

• Describe pain patterns and relief strategies.
• Note vomitus characteristics (bright red, coffee grounds, undigested food).
• Ask about bloody or tarry stools.
• List usual food intake.
• Assess lifestyle habits (smoking, alcohol, NSAID use).
• Assess vital signs (tachycardia, hypotension).
• Test stool for occult blood.
• Palpate abdomen for tenderness.

Nursing Process: Diagnosis

• Acute pain associated with gastric acid.
• Anxiety related to the acute illness.
• Impaired nutritional intake.
• Potential complications include: Hemorrhage, Perforation, Penetration, Gastric outlet obstruction

Nursing Process: Planning and Goals

• Relief of pain.
• Reduced anxiety.
• Maintenance of nutritional requirements.
• Absence of complications.

Nursing Process: Interventions:Relieving Pain

• With prescribed medications, the patient should avoid NSAIDs, aspirin in particular, as well as alcohol.
• In addition, meals should be eaten at regularly paced intervals in a relaxed setting.
• Some patients benefit from learning relaxation techniques to help manage stress and pain.

Reducing Anxiety

• Assess the patient’s level of anxiety.
• Explain diagnostic tests and administer medications as scheduled.
• Helps identify stressors.
• Explain various coping techniques and relaxation methods.
• The patient’s family is also encouraged to participate in care and to provide emotional support.

Maintaining Optimal Nutritional Status

• Assess the patient for malnutrition and weight loss.
• Assess the patient about the importance of adhering to the medication regimen and dietary restriction.

Monitoring and Managing Potential Complications

Hemorrhage

• The vomited blood can be bright red, or it can have a dark coffee grounds appearance from the oxidation of hemoglobin to methemoglobin.
• If hemorrhage is large, blood is vomited. With small hemorrhage, blood is passed in tarry black stools.
• Management depends on the amount of blood lost and the rate of bleeding.
• The nurse must monitor vital signs frequently and evaluate the patient for tachycardia, hypotension, and tachypnea.
• Management involves monitoring hemoglobin, hematocrit, testing stool for blood, and recording hourly urine output.
• Endoscopic interventions include injecting epinephrine or alcohol, cauterizing, or clipping bleeding sites.
• Patients suspected of having an ulcer who present with symptoms of acute GI bleeding should undergo evaluation with endoscopy within 12 h
• Many patients also undergo procedures (e.g., vagotomy and pyloroplasty, gastrectomy) aimed at controlling the underlying cause of the ulcers.
• Transcatheter Arterial Embolization (TAE) involves inserting a catheter into an artery to occlude blood flow to the bleeding vessel.
• If GI bleeding occurs, collaborative treatment guidelines for hemorrhagic shock must be followed.
• Insert an NG tube to distinguish fresh blood from coffee grounds, aid in removal of clots and acid through saline lavage, prevent nausea/vomiting through suction decompression

Perforation and Penetration

• Perforation is the erosion of the ulcer through the gastric serosa into the peritoneal cavity without warning.
• Penetration is erosion of the ulcer through the gastric serosa into adjacent structures such as the pancreas, biliary tract, or gastrohepatic omentum.
• Signs and symptoms of perforation include-Sudden, severe upper abdominal pain, Vomiting, Collapse, Extremely tender and rigid abdomen, Hypotension and tachycardia, indicating shock
• Because chemical peritonitis develops within a few hours of perforation and is followed by bacterial peritonitis, the perforation must be closed as quickly as possible and the abdominal cavity lavaged of stomach or intestinal contents.

Overview of gastrointestinal conditions such as achlorhydria, antrectomy and dumping syndrome. Includes definitions of dyspepsia, gastritis and gastric outlet obstruction. Also covers Helicobacter pylori (H. pylori).