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Peptic Ulcer Disease: A Comprehensive Guide to Differential Diagnosis

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Introduction

Peptic ulcer disease (PUD) refers to sores that develop on the lining of the stomach, lower esophagus, or small intestine. These ulcers occur when the protective mucus lining breaks down, often due to factors such as Helicobacter pylori (H. pylori) infection or prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs). Characterized by a disruption in the gastrointestinal (GI) tract lining caused by gastric acid and pepsin, PUD extends into the muscularis propria layer. While commonly found in the stomach and proximal duodenum, ulcers can also manifest in the lower esophagus, distal duodenum, or jejunum. Patients typically experience epigastric pain, with gastric ulcer pain appearing shortly after meals and duodenal ulcer pain emerging a few hours later. Modern management emphasizes H. pylori testing and proton pump inhibitor (PPI)-based triple therapy, but accurate diagnosis is paramount. This article aims to provide a detailed understanding of PUD, with a particular focus on its differential diagnosis, ensuring clinicians can effectively distinguish it from other conditions presenting with similar symptoms. Recognizing the nuances of differential diagnosis is crucial for timely and appropriate patient management, preventing potential complications and optimizing treatment strategies.

Etiology

Peptic ulcer disease arises from a variety of factors, with the majority of cases linked to Helicobacter pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Understanding the diverse etiologies is essential for targeted prevention and treatment strategies.

Common Causes of Peptic Ulcer Disease:

  • H. pylori Infection: This bacterium is a leading cause, implicated in a significant proportion of both duodenal and gastric ulcers.
  • NSAIDs: These commonly used pain relievers inhibit prostaglandin production, compromising the protective lining of the stomach and duodenum.
  • Medications: Certain other medications, beyond NSAIDs, can also increase the risk of PUD.

Less Common Causes of Peptic Ulcer Disease:

  • Zollinger-Ellison Syndrome: A rare condition characterized by excessive gastrin production, leading to severe acid secretion and ulcers.
  • Malignancy: Gastric, lung cancers, and lymphomas can, in rare instances, present with or mimic peptic ulcer disease.
  • Stress Ulcers: Physiological stress from acute illness, burns, or head injuries can lead to stress-related mucosal damage and ulceration.
  • Viral Infections: Certain viral infections have been associated with PUD in immunocompromised individuals.
  • Vascular Insufficiency: Reduced blood flow to the gastric mucosa can impair its integrity and increase ulcer risk.
  • Radiation Therapy: Radiation to the abdomen can damage the GI lining.
  • Crohn’s Disease: This inflammatory bowel disease can sometimes involve the upper GI tract, leading to peptic ulcers.
  • Chemotherapy: Certain chemotherapy agents can cause mucosal damage and ulceration as a side effect.

Helicobacter Pylori-Associated PUD

H. pylori, a gram-negative bacterium, colonizes the gastric epithelium and is a major global health concern. It’s responsible for a large percentage of duodenal ulcers (around 90%) and a significant portion of gastric ulcers (70-90%). Infection rates are higher in populations with lower socioeconomic status and are often acquired in childhood. H. pylori possesses several virulence factors that enable it to thrive in the harsh gastric environment and induce mucosal damage.

Key Virulence Factors of Helicobacter Pylori:

  1. Urease: This enzyme breaks down urea into ammonia, neutralizing stomach acid and creating a protective microenvironment for the bacteria.
  2. Toxins (CagA/VacA): These toxins contribute to mucosal inflammation and tissue damage, playing a role in ulcer development.
  3. Flagella: These whip-like appendages provide motility, allowing H. pylori to move through the gastric mucus and reach the epithelial cells.

NSAID-Associated PUD

NSAIDs are the second most frequent cause of PUD. Prostaglandins normally protect the gastric mucosa by promoting mucus and bicarbonate secretion, and maintaining mucosal blood flow. NSAIDs inhibit cyclooxygenase-1 (COX-1), an enzyme crucial for prostaglandin synthesis. This inhibition reduces prostaglandin levels, weakening mucosal defense and increasing susceptibility to acid and pepsin damage.

Medication-Induced PUD

Besides NSAIDs, other medications have been linked to PUD, including corticosteroids, bisphosphonates, potassium chloride supplements, and fluorouracil. These agents can compromise mucosal integrity through various mechanisms.

Lifestyle factors also play a role. Smoking is associated with an increased risk of duodenal ulcers, although the relationship isn’t fully understood. Alcohol can irritate the gastric mucosa and increase acid secretion, potentially contributing to ulcer formation.

Conditions leading to a hypersecretory environment, increasing gastric acid production and ulcer risk, include Zollinger-Ellison syndrome, systemic mastocytosis, cystic fibrosis, hyperparathyroidism, and antral G cell hyperplasia.

Epidemiology

Peptic ulcer disease is a widespread global health issue, affecting millions worldwide. The lifetime risk of developing PUD is estimated to be between 5% and 10%. However, the incidence of PUD has been declining globally due to improved sanitation, hygiene practices, effective treatments for H. pylori, and more judicious use of NSAIDs.

Duodenal ulcers are approximately four times more common than gastric ulcers. Furthermore, duodenal ulcers are more frequently observed in men compared to women. While the overall prevalence is decreasing, PUD remains a significant cause of morbidity and healthcare utilization.

Pathophysiology

The development of peptic ulcer disease is fundamentally due to an imbalance between protective and aggressive factors in the gastroduodenal mucosa. Aggressive factors, such as gastric acid and pepsin, can overwhelm the mucosal defenses, leading to ulceration. Conversely, protective factors, including mucus and bicarbonate secretion, prostaglandin synthesis, mucosal blood flow, and cellular restitution, normally maintain mucosal integrity.

Risk Factors Predisposing to PUD:

  • H. pylori infection: Disrupts mucosal defense and promotes inflammation.
  • NSAID use: Inhibits prostaglandin synthesis, reducing mucosal protection.
  • Family history of PUD: Genetic predisposition may play a role.
  • Immigration from a developing nation: Higher prevalence of H. pylori in some regions.
  • African American/Hispanic ethnicity: Some studies suggest higher incidence in these groups.

In PUD, the mucosal defect extends through the muscularis mucosa, breaching the protective superficial layer. This exposes the underlying tissue to gastric acid and pepsin, perpetuating the ulcer and hindering healing. H. pylori infection further disrupts mucosal defense by impairing bicarbonate secretion and inducing inflammation, creating an environment conducive to ulcer formation.

Histopathology

The gross and microscopic features of peptic ulcers provide valuable diagnostic information. Gastric ulcers are predominantly found on the lesser curvature of the stomach, while duodenal ulcers are most commonly located in the duodenal bulb, the first part of the duodenum.

Macroscopically, ulcers appear as round to oval lesions with a smooth base. Acute ulcers typically exhibit regular, sharply demarcated borders. Chronic ulcers, in contrast, often have elevated, thickened borders due to surrounding inflammation and fibrosis. Histologically, a peptic ulcer is characterized by its depth, extending beyond the muscularis mucosa into deeper layers of the gastric or duodenal wall. Microscopic examination reveals distinct zones within the ulcer crater, including a necrotic zone, an inflammatory zone, granulation tissue, and fibrosis in chronic ulcers.

History and Physical Examination

The clinical presentation of peptic ulcer disease can vary depending on the ulcer location (gastric vs. duodenal) and patient age. Symptom timing in relation to meals is a key differentiator between gastric and duodenal ulcers. Nocturnal pain is particularly common in duodenal ulcers, often awakening patients at night. Patients with gastric outlet obstruction, a complication of PUD, may report abdominal bloating and fullness, early satiety, and vomiting.

Common Signs and Symptoms of PUD:

  • Epigastric abdominal pain: The hallmark symptom, often described as burning or gnawing.
  • Bloating: A feeling of fullness and distention in the abdomen.
  • Abdominal fullness: Feeling full quickly after eating, or persistently full.
  • Nausea and vomiting: May occur, especially in gastric outlet obstruction.
  • Weight loss or weight gain: Weight loss is more common with gastric ulcers (due to pain exacerbated by eating), while weight gain can occur with duodenal ulcers (pain relieved by eating).
  • Hematemesis: Vomiting blood, indicating upper GI bleeding.
  • Melena: Black, tarry stools, indicating digested blood from upper GI bleeding.

Alarm Symptoms (Warning Signs) Requiring Urgent Referral:

  • Unintentional weight loss: Suggestive of malignancy or significant underlying disease.
  • Progressive dysphagia: Difficulty swallowing, may indicate esophageal cancer or stricture.
  • Overt gastrointestinal bleeding: Hematemesis or melena, indicating significant ulcer complications.
  • Iron deficiency anemia: Can be caused by chronic blood loss from an ulcer.
  • Recurrent emesis: Persistent vomiting, may indicate gastric outlet obstruction or other serious conditions.
  • Family history of upper gastrointestinal malignancy: Increased risk of gastric cancer.

Evaluation and Diagnosis

Diagnosing PUD involves a comprehensive approach, integrating patient history, physical examination, and diagnostic tests. A detailed history, focusing on symptom characteristics, timing, and associated factors, is crucial. Physical examination may reveal epigastric tenderness and signs of anemia in cases of bleeding.

Diagnostic Investigations for PUD:

  1. Esophagogastroduodenoscopy (EGD): This is the gold standard diagnostic test for PUD, offering high sensitivity and specificity (up to 90%) for detecting both gastric and duodenal ulcers. EGD allows for direct visualization of the mucosa, biopsy sampling to rule out malignancy and assess for H. pylori, and therapeutic intervention if needed. Guidelines recommend EGD for patients over 50 with new-onset dyspepsia and for any patient with alarm symptoms.

  2. Barium Swallow: An alternative imaging test when EGD is contraindicated. While less sensitive than EGD, it can detect ulcers and gastric outlet obstruction.

  3. Laboratory Tests:

    • Complete blood count (CBC): To assess for anemia.
    • Liver function tests (LFTs): Generally normal in uncomplicated PUD, but helpful in differential diagnosis.
    • Amylase and lipase levels: To rule out pancreatitis in patients with epigastric pain.
    • Serum gastrin level: Ordered if Zollinger-Ellison syndrome is suspected (elevated gastrin levels).

  4. Helicobacter pylori Testing: Essential for identifying H. pylori-related PUD. Various non-invasive and invasive tests are available:

    • Serologic testing (blood test): Detects H. pylori antibodies, indicating past or current infection. Not useful for confirming eradication after treatment.
    • Urea breath test (UBT): Highly sensitive and specific non-invasive test. Detects H. pylori urease activity. Can also confirm eradication post-treatment.
    • Stool antigen test: Another non-invasive test with good sensitivity and specificity for detecting active H. pylori infection. Useful for diagnosis and eradication confirmation.
    • Urine-based ELISA and rapid urine test: Less commonly used, but available non-invasive options.
    • Endoscopic biopsy: Invasive, obtained during EGD. Allows for histological examination, rapid urease test (CLO test), and culture (if antibiotic resistance is suspected). Biopsies should be taken from multiple sites (at least 4-6) to increase sensitivity, especially for gastric ulcers to rule out malignancy.

  5. Computerized Tomography (CT) of the Abdomen with Contrast: Not typically used for diagnosing uncomplicated PUD itself. However, CT is valuable in evaluating complications such as perforation, gastric outlet obstruction, or in differentiating PUD from other abdominal conditions.

Treatment and Management

The primary goals of PUD treatment are to relieve symptoms, promote ulcer healing, prevent recurrence, and eradicate H. pylori infection when present. Medical management is the mainstay of treatment, with surgery reserved for refractory cases or complications.

Medical Treatment:

  • Antisecretory Medications:

    • Proton Pump Inhibitors (PPIs): These are the most potent acid-suppressing drugs and have largely replaced H2-receptor antagonists due to superior efficacy in healing ulcers and relieving symptoms. PPIs (e.g., omeprazole, pantoprazole, lansoprazole, esomeprazole, rabeprazole) block gastric acid production. Long-term PPI use may be associated with an increased risk of bone fractures, and calcium supplementation may be considered.
    • H2-Receptor Antagonists (H2RAs): (e.g., ranitidine, famotidine, cimetidine) Reduce acid secretion, but less potent than PPIs. Less commonly used as first-line therapy now.

  • H. pylori Eradication Therapy: For H. pylori-positive PUD, eradication is crucial to prevent recurrence. First-line therapy is typically a triple regimen consisting of two antibiotics and a PPI, administered for 7 to 14 days. Common regimens include:

    • PPI + clarithromycin + amoxicillin
    • PPI + clarithromycin + metronidazole (for penicillin-allergic patients)
      Antibiotic selection should consider local antibiotic resistance patterns. If first-line therapy fails, quadruple therapy with bismuth, metronidazole, tetracycline, and a PPI is often used.

  • NSAID-Induced PUD Management:

    • Discontinue NSAID use if possible.
    • If NSAIDs must be continued, switch to the lowest effective dose or a COX-2 selective NSAID (celecoxib), which has a lower risk of GI side effects (though cardiovascular risks should be considered).
    • Prophylactic prostaglandin analogs (misoprostol) or PPIs can be used to reduce ulcer risk in patients requiring chronic NSAID therapy.

  • Other Medications: Discontinue or minimize use of other ulcerogenic medications if possible (corticosteroids, bisphosphonates, anticoagulants).

Refractory PUD and Surgical Treatment:

A refractory peptic ulcer is defined as an ulcer (>5mm in diameter) that fails to heal despite 8-12 weeks of PPI therapy. Causes include persistent H. pylori infection, continued NSAID use, comorbidities impairing healing, Zollinger-Ellison syndrome, or gastric cancer. If refractory ulcers persist after addressing these factors, surgical intervention may be considered.

Surgical options for PUD are now less common due to effective medical therapies but remain important for complications or refractory disease:

  • Vagotomy: Severing the vagus nerve to reduce gastric acid secretion.
  • Partial gastrectomy: Removal of a portion of the stomach, may be necessary for bleeding ulcers unresponsive to endoscopic therapy or for gastric outlet obstruction.

Differential Diagnosis

Peptic ulcer disease shares symptom overlap with several other conditions, making differential diagnosis crucial for accurate management. It is important to consider and rule out these conditions to ensure patients receive appropriate and timely treatment.

Conditions to Consider in the Differential Diagnosis of Peptic Ulcer Disease:

  1. Gastritis: Inflammation of the gastric mucosa, often caused by H. pylori, NSAIDs, alcohol, or autoimmune conditions. Differentiation: Gastritis and PUD can present with similar epigastric pain and nausea. Endoscopy is often needed for definitive diagnosis. Gastritis typically shows mucosal inflammation without deep ulceration seen in PUD. Biopsy during endoscopy helps distinguish between the two.

  2. Gastroesophageal Reflux Disease (GERD): Characterized by heartburn and acid regurgitation due to stomach acid reflux into the esophagus. Differentiation: GERD pain is typically a burning sensation in the epigastrium or retrosternal area, often exacerbated by lying down or after meals. While PUD pain can also be postprandial, it’s often described as gnawing or aching. GERD is less likely to cause weight loss or vomiting, unless complicated by esophagitis or stricture. Endoscopy can differentiate by visualizing esophageal inflammation in GERD and gastric/duodenal ulcers in PUD.

  3. Gastric Cancer: Malignant tumors of the stomach lining. Differentiation: Gastric cancer can present with epigastric pain, but often accompanied by prominent alarm symptoms like unintentional weight loss, anorexia, early satiety, persistent vomiting, and GI bleeding (hematemesis, melena). Older age, family history of gastric cancer, and new-onset dyspepsia in older individuals raise suspicion. Endoscopy with biopsy is essential for definitive diagnosis.

  4. Pancreatitis: Inflammation of the pancreas, commonly caused by gallstones or alcohol abuse. Differentiation: Pancreatitis typically presents with severe, persistent epigastric or right upper quadrant pain that often radiates to the back. Pain is often worse in the supine position and may be relieved by sitting or leaning forward. Nausea, vomiting, and fever are common. Elevated serum amylase and lipase levels are diagnostic markers. CT scan of the abdomen is often used to confirm pancreatitis and assess severity. PUD pain is less likely to be constant and severe, and amylase/lipase are usually normal.

  5. Biliary Colic: Transient pain caused by gallstones obstructing the bile duct. Differentiation: Biliary colic is characterized by intermittent, severe, cramping pain in the right upper quadrant or epigastrium, often precipitated by fatty meals. Pain typically lasts from minutes to hours and resolves spontaneously. Physical exam may be normal between episodes. Ultrasound of the gallbladder is the primary diagnostic tool. PUD pain is generally more persistent and less directly related to fatty food intake.

  6. Cholecystitis: Inflammation of the gallbladder, usually due to gallstone obstruction of the cystic duct. Differentiation: Cholecystitis presents with more prolonged and constant right upper quadrant or epigastric pain compared to biliary colic, often lasting for hours. Pain is exacerbated by fatty meals and associated with nausea, vomiting, and fever. Physical exam findings may include right upper quadrant tenderness and a positive Murphy’s sign. Leukocytosis and abnormal liver function tests can also be present. Ultrasound or HIDA scan are used for diagnosis. PUD pain is less likely to be associated with fever, Murphy’s sign, or abnormal LFTs.

  7. Acute Myocardial Infarction (AMI): Heart attack, especially inferior MI, can sometimes present with epigastric pain, mimicking PUD. Differentiation: AMI-related epigastric pain may be associated with chest pain, shortness of breath, sweating, and nausea. Risk factors for coronary artery disease (e.g., hypertension, hyperlipidemia, smoking, diabetes) should raise suspicion. ECG and cardiac biomarkers (troponin) are crucial for diagnosing AMI. PUD pain is typically not associated with ECG changes or elevated troponin. It’s critical to consider cardiac causes in patients presenting with epigastric pain, especially those at risk for heart disease.

  8. Mesenteric Ischemia: Reduced blood flow to the intestines, which can be acute or chronic. Differentiation: Acute mesenteric ischemia is a surgical emergency characterized by severe, diffuse abdominal pain that is often out of proportion to physical exam findings. Risk factors include older age, atrial fibrillation, and atherosclerosis. Chronic mesenteric ischemia presents with postprandial abdominal pain (“intestinal angina”), weight loss, and food aversion. CT angiography is the diagnostic test of choice. PUD pain is less likely to be as severe and disproportionate to exam findings in acute ischemia, or associated with food aversion and weight loss in chronic ischemia.

  9. Functional Dyspepsia: Chronic upper abdominal pain or discomfort without identifiable organic disease (after upper endoscopy). Differentiation: Functional dyspepsia is a diagnosis of exclusion. Patients present with dyspeptic symptoms (epigastric pain, burning, fullness, nausea) but EGD is normal, ruling out PUD, gastritis, and esophagitis. Symptoms may overlap with PUD, but the absence of ulcers on endoscopy is key. Functional dyspepsia is often related to altered gastric motility, visceral hypersensitivity, and psychosocial factors.

  10. Medication-Induced Gastritis/Esophagitis (Non-NSAID): Certain medications other than NSAIDs can cause upper GI symptoms. Differentiation: Medications like bisphosphonates, potassium chloride, iron supplements, and some antibiotics can cause gastritis or esophagitis. A thorough medication history is important. Symptoms may mimic PUD or GERD. Discontinuation of the offending medication often leads to symptom resolution. Endoscopy may show mucosal inflammation or erosions.

Distinguishing PUD from these conditions requires careful history taking, physical examination, appropriate investigations, and a high index of clinical suspicion, especially for serious conditions like AMI and mesenteric ischemia.

Prognosis

The prognosis for peptic ulcer disease is generally excellent when the underlying cause is effectively treated. H. pylori eradication therapy significantly reduces the risk of ulcer recurrence in H. pylori-positive patients. Avoiding NSAIDs, smoking, and excessive alcohol consumption also contributes to preventing recurrence.

However, PUD recurrence remains a concern, with reported rates exceeding 60% in some studies, particularly in patients who continue to use NSAIDs or fail to eradicate H. pylori. NSAID-induced gastric perforation, a serious complication, occurs at a rate of approximately 0.3% per patient per year in chronic NSAID users. Despite the potential for recurrence and complications, mortality rates associated with peptic ulcer disease have significantly decreased in recent decades due to advancements in diagnosis and treatment.

Complications

If left undiagnosed or untreated, peptic ulcer disease can lead to serious and potentially life-threatening complications. Prompt diagnosis and appropriate management are essential to prevent these sequelae.

Potential Complications of PUD:

  • Upper Gastrointestinal Bleeding: The most common complication, ranging from mild anemia to life-threatening hemorrhage (hematemesis, melena).
  • Gastric Outlet Obstruction: Scarring and edema from chronic ulcers in the pyloric channel or duodenal bulb can narrow or block the gastric outlet, leading to vomiting, abdominal distention, and dehydration.
  • Perforation: Ulcer penetration through the entire stomach or duodenal wall, leading to peritonitis, a surgical emergency characterized by severe abdominal pain, rigidity, and sepsis.
  • Penetration: Ulcer extension into adjacent organs, such as the pancreas or liver, causing chronic pain and potential organ dysfunction.
  • Gastric Cancer: Chronic gastric ulcers, particularly those associated with H. pylori, have a slightly increased risk of malignant transformation into gastric adenocarcinoma. Regular endoscopic surveillance may be recommended for certain gastric ulcers.

Deterrence and Patient Education

Preventing peptic ulcer disease and its recurrence involves lifestyle modifications and patient education. Patients should be counseled about risk factors and strategies to minimize their risk.

Key Deterrence and Patient Education Points:

  • Avoid or minimize NSAID use: Discuss alternative pain management options with healthcare providers if chronic pain is a concern. If NSAIDs are necessary, use the lowest effective dose for the shortest duration, and consider gastroprotective agents (PPIs or misoprostol) for high-risk individuals.
  • Smoking cessation: Smoking impairs ulcer healing and increases recurrence risk.
  • Limit alcohol consumption: Excessive alcohol can irritate the gastric mucosa.
  • Reduce caffeine intake: Caffeine can stimulate acid secretion in some individuals.
  • Weight management: Obesity has been associated with increased PUD risk.
  • Stress reduction techniques: Stress may exacerbate PUD symptoms in some patients.
  • H. pylori eradication: Complete recommended eradication therapy if H. pylori infection is diagnosed.
  • Medication adherence: Emphasize the importance of taking prescribed medications (PPIs, antibiotics) as directed for optimal healing and H. pylori eradication.
  • Recognize alarm symptoms: Educate patients about alarm symptoms (unintentional weight loss, dysphagia, bleeding, anemia, persistent vomiting) and advise them to seek prompt medical attention if these occur.

Pearls and Other Issues

  • Ulcer vs. Erosion: Lesions smaller than 5 mm in diameter are termed erosions, while those larger than 5 mm are classified as ulcers. Both involve mucosal breaks, but ulcers are deeper.
  • COX-2 Selective NSAIDs: These agents (e.g., celecoxib) are less likely to cause PUD compared to non-selective NSAIDs because COX-2 is less expressed in the gastric mucosa. However, they still carry cardiovascular risks and should be used cautiously, especially in patients with prior PUD or cardiovascular disease.
  • Zollinger-Ellison Syndrome (Gastrinoma): Suspect this condition in patients with multiple or refractory ulcers, ulcers in unusual locations (distal duodenum, jejunum), diarrhea, or hypercalcemia. Diagnosis is confirmed by elevated serum gastrin levels and imaging to locate the gastrin-producing tumor (gastrinoma), often in the pancreas or duodenum.

Enhancing Healthcare Team Outcomes

Optimal management of peptic ulcer disease requires a collaborative, evidence-based interprofessional team approach. PUD is a common condition encountered in various healthcare settings, including primary care, emergency departments, urgent care clinics, and outpatient gastroenterology practices. Effective communication and coordination among healthcare professionals are essential to ensure accurate diagnosis, timely treatment, and patient education.

Strategies for Enhancing Healthcare Team Outcomes in PUD Management:

  • Awareness and Vigilance: All healthcare team members, including physicians, nurses, pharmacists, and dietitians, should be aware of PUD and its varied presentations. Nurses play a crucial role in patient assessment, monitoring, education, and communication with the team. Recognizing that abdominal pain can mimic other pathologies is important to avoid delays in diagnosis and treatment.
  • Patient Education: Comprehensive patient education is paramount. This includes lifestyle modifications (smoking cessation, alcohol and caffeine limitation, NSAID avoidance), medication compliance, and recognition of alarm symptoms. Pharmacists play a key role in medication reconciliation and patient counseling on appropriate medication use and potential side effects.
  • Dietary Consultation: Registered dietitians can provide guidance on dietary modifications, especially for patients with symptoms exacerbated by food or those needing weight management.
  • Multidisciplinary Approach to Refractory Cases: For patients with refractory ulcers or complications, a multidisciplinary team involving gastroenterologists, surgeons, radiologists, and other specialists may be necessary to optimize management strategies.
  • Evidence-Based Protocols: Implementing and adhering to evidence-based guidelines for PUD diagnosis and treatment ensures consistent and high-quality care.
  • Regular Communication and Handovers: Effective communication among team members, especially during patient handovers between different care settings, is crucial to maintain continuity of care and avoid errors.

By fostering a collaborative and informed healthcare team, patient outcomes in peptic ulcer disease can be significantly improved, reducing morbidity and optimizing long-term management. For most patients treated with appropriate medical therapy and H. pylori eradication when indicated, the prognosis is excellent, but vigilance for recurrence and complications remains important.

Review Questions

(Review questions from the original article can be included here if desired, or new questions relevant to differential diagnosis can be added)

References

(Keep the original references from the article)

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