Peptic & Duodenal Ulcers
Comprehensive Nursing Education Notes
Table of Contents
Introduction & Overview
Definition
Peptic ulcer disease (PUD) is a condition characterized by painful sores or ulcers that develop in the lining of the stomach (gastric ulcers) or the first part of the small intestine, called the duodenum (duodenal ulcers). These ulcers form when the protective mucous layer is compromised, allowing digestive acids to erode the underlying tissue.
Anatomical illustration showing gastric and duodenal ulcers with H. pylori bacteria
Key Statistics
- • Affects 10-15% of the global population
- • Duodenal ulcers are 4x more common than gastric ulcers
- • Peak incidence: 30-60 years of age
- • Male-to-female ratio: 3:1 for duodenal ulcers
Prognosis
- • 90-95% healing rate with proper treatment
- • Low recurrence with H. pylori eradication
- • Most ulcers heal within 4-8 weeks
- • Excellent prognosis when managed appropriately
Anatomy & Pathophysiology
Gastric Anatomy Review
Stomach Layers (Inside to Outside)
- Mucosa: Innermost layer with epithelial cells
- Submucosa: Contains blood vessels and nerves
- Muscularis: Smooth muscle layer
- Serosa: Outermost protective layer
Duodenal Anatomy
- • Length: 25-30 cm (10-12 inches)
- • Parts: Superior, descending, horizontal, ascending
- • pH: Highly acidic initially (1.5-3.5)
- • Function: Primary site of digestion and absorption
Protective Mechanisms
Mucus Barrier
Alkaline mucus neutralizes acid
Rapid Regeneration
Epithelial cells renew every 3-5 days
Blood Flow
Adequate perfusion maintains tissue health
Pathophysiological Imbalance
Peptic ulcers develop when aggressive factors overwhelm protective mechanisms:
Aggressive Factors ⚡
- • Gastric acid (HCl)
- • Pepsin enzyme
- • H. pylori bacteria
- • NSAIDs
- • Alcohol
- • Bile acids
Protective Factors 🛡️
- • Mucus secretion
- • Bicarbonate production
- • Prostaglandin E2
- • Adequate blood flow
- • Epithelial regeneration
- • Growth factors
Types of Peptic Ulcers
Gastric Ulcers
Location:
Stomach lining, typically in the antrum or lesser curvature
Characteristics:
- • More common in older adults (50-70 years)
- • Equal gender distribution
- • Pain occurs with eating
- • Higher risk of malignancy
- • Associated with H. pylori (60-70%)
Pain Pattern:
Epigastric pain that worsens with food intake
Duodenal Ulcers
Location:
First portion of duodenum, within 3cm of pylorus
Characteristics:
- • More common in younger adults (20-50 years)
- • Male predominance (3:1 ratio)
- • Pain relieved by eating
- • Rarely malignant
- • Strongly associated with H. pylori (90-95%)
Pain Pattern:
Epigastric pain that improves with food, worsens when hungry
Classification by Depth
Superficial
Mucosa only
Deep
Into submucosa
Penetrating
Through muscularis
Perforating
Through serosa
Etiology & Risk Factors
Primary Causes
Helicobacter pylori
Primary bacterial cause
- • Prevalence: 60% of gastric, 90% of duodenal ulcers
- • Transmission: Oral-oral, fecal-oral routes
- • Mechanism: Produces urease, damages mucosa
- • Testing: Urea breath test, stool antigen, biopsy
- • Treatment: Triple or quadruple therapy
NSAIDs
Non-steroidal anti-inflammatory drugs
- • Mechanism: Inhibits COX-1, reduces prostaglandin E2
- • Risk factors: Age >65, high dose, prolonged use
- • Common drugs: Aspirin, ibuprofen, naproxen
- • Prevention: PPIs, H2 blockers with NSAIDs
- • Alternatives: COX-2 selective inhibitors
Risk Factor Categories
Patient Factors
- • Age extremes (<10, >65 years)
- • Male gender (duodenal)
- • Blood type O (duodenal)
- • Family history
- • Genetic factors
- • Comorbid conditions
Lifestyle Factors
- • Smoking (doubles risk)
- • Alcohol consumption
- • Stress (acute/chronic)
- • Irregular eating patterns
- • Spicy food (controversial)
- • Poor dietary habits
Medical Factors
- • Zollinger-Ellison syndrome
- • Crohn’s disease
- • Hypercalcemia
- • Mechanical ventilation
- • Burns (Curling ulcers)
- • Head trauma (Cushing ulcers)
Medication-Induced Ulcers
High-Risk Medications
- • Corticosteroids: When combined with NSAIDs
- • Anticoagulants: Warfarin, heparin
- • Bisphosphonates: Alendronate, risedronate
- • Chemotherapy: Various cytotoxic agents
Protective Strategies
- • Co-prescribe PPIs with high-risk medications
- • Use lowest effective dose
- • Consider alternative medications
- • Regular monitoring and assessment
Pathogenesis
H. pylori Pathogenesis Flowchart
H. pylori Infection
Bacteria colonizes gastric mucus layer
Urease Production
Converts urea to ammonia, neutralizes acid
Inflammatory Response
Neutrophil infiltration, cytokine release
Mucosal Damage
Epithelial cell death, barrier disruption
Ulcer Formation
Acid exposure leads to tissue erosion
NSAID-Induced Pathogenesis
Direct Effects
- • Topical irritation of gastric mucosa
- • Disruption of mucosal barrier
- • Increased back-diffusion of H+ ions
- • Direct cellular toxicity
Indirect Effects
- • COX-1 inhibition
- • Reduced prostaglandin E2 synthesis
- • Decreased mucus and bicarbonate production
- • Impaired mucosal blood flow
Molecular Mechanisms
Genetic Factors
IL-1β, TNF-α polymorphisms affect inflammatory response
Virulence Factors
CagA, VacA proteins increase pathogenicity
Host Defense
Immune response determines infection outcome
Clinical Manifestations
Primary Symptoms
Epigastric Pain
Characteristics:
- • Burning, gnawing, or aching sensation
- • Located in upper abdomen, below sternum
- • May radiate to back or chest
- • Intensity varies from mild to severe
Timing Patterns:
- • Gastric ulcers: Pain with meals
- • Duodenal ulcers: Pain 2-3 hours after meals
- • Night pain: Common with duodenal ulcers
- • Relief: Antacids, food (duodenal)
Gastrointestinal Symptoms
- • Dyspepsia: Indigestion, bloating, fullness
- • Nausea and vomiting: Especially with gastric ulcers
- • Appetite changes: Loss of appetite, early satiety
- • Weight loss: Due to fear of eating (gastric ulcers)
- • Heartburn: Acid reflux symptoms
- • Belching: Excessive gas production
Atypical Presentations
Elderly Patients
- • Silent ulcers (no pain)
- • Complications as first presentation
- • Vague abdominal discomfort
- • Bleeding without warning signs
NSAID Users
- • Minimal or no symptoms
- • Higher complication rates
- • Sudden onset of bleeding
- • Perforation without warning
Diabetic Patients
- • Neuropathy masks pain
- • Delayed gastric emptying
- • Poor wound healing
- • Increased infection risk
Red Flag Symptoms – Immediate Medical Attention Required
Gastrointestinal Bleeding
- • Hematemesis: Vomiting blood or coffee-ground material
- • Melena: Black, tarry stools
- • Hematochezia: Bright red blood in stool (severe bleeding)
- • Occult bleeding: Positive fecal occult blood test
Other Emergency Signs
- • Severe abdominal pain: Sudden, intense pain
- • Perforation signs: Board-like rigidity
- • Shock symptoms: Hypotension, tachycardia
- • Anemia symptoms: Fatigue, weakness, pallor
Diagnostic Methods
Diagnostic Approach Flowchart
Patient Presentation
Dyspepsia, epigastric pain
Initial Assessment
History, physical exam, red flags
Age < 55, No Red Flags
H. pylori testing first
Age ≥ 55, Red Flags
Urgent endoscopy
Laboratory Tests
H. pylori Testing
Non-invasive Tests:
- • Urea Breath Test: Gold standard, 95% accuracy
- • Stool Antigen Test: Good sensitivity/specificity
- • Serology: IgG antibodies, less reliable
Invasive Tests:
- • Rapid Urease Test: During endoscopy
- • Histology: Tissue examination
- • Culture: For antibiotic sensitivity
Other Laboratory Tests
- • Complete Blood Count: Anemia from bleeding
- • Iron Studies: Iron deficiency anemia
- • Liver Function Tests: Medication monitoring
- • Serum Gastrin: Zollinger-Ellison syndrome
- • Fecal Occult Blood: Hidden bleeding
- • Electrolytes: Complications assessment
Imaging Studies
Upper Endoscopy (EGD)
- • Gold standard for diagnosis
- • Direct visualization of ulcers
- • Biopsy capability
- • Therapeutic interventions
- • 95-99% sensitivity
Upper GI Series
- • Barium contrast study
- • Less invasive option
- • 80-90% sensitivity
- • Cannot obtain tissue
- • Used when endoscopy unavailable
CT Scan
- • Complications assessment
- • Perforation detection
- • Free air identification
- • Not for routine diagnosis
- • Emergency situations
Endoscopic Classification
Forrest Classification (Bleeding Risk)
- • Ia: Active spurting bleeding
- • Ib: Active oozing bleeding
- • IIa: Non-bleeding visible vessel
- • IIb: Adherent clot
- • IIc: Flat pigmented spot
- • III: Clean base
Endoscopic Features
- • Size: Measured in millimeters
- • Depth: Mucosal vs. deeper layers
- • Location: Anatomical site description
- • Surrounding mucosa: Inflammation, scarring
- • Complications: Bleeding, perforation signs
Treatment & Management
Treatment Algorithm
H. pylori Positive
- • PPI (omeprazole 20mg BID)
- • Amoxicillin 1g BID
- • Clarithromycin 500mg BID
- • PPI + Bismuth + Tetracycline + Metronidazole
H. pylori Negative
- • Discontinue NSAID if possible
- • PPI therapy 4-8 weeks
- • Switch to COX-2 inhibitor
- • PPI therapy 4-8 weeks
- • Long-term maintenance if needed
Medication Classes
Proton Pump Inhibitors (PPIs)
Mechanism:
Irreversibly block H+/K+-ATPase enzyme
Common Agents:
- • Omeprazole: 20-40mg daily
- • Lansoprazole: 15-30mg daily
- • Esomeprazole: 20-40mg daily
- • Pantoprazole: 40mg daily
Side Effects:
Hypomagnesemia, C. diff risk, fractures (long-term)
H2 Receptor Antagonists
Mechanism:
Block histamine H2 receptors on parietal cells
Common Agents:
- • Ranitidine: 150mg BID (withdrawn)
- • Famotidine: 20-40mg BID
- • Cimetidine: 400mg BID
- • Nizatidine: 150mg BID
Uses:
Less potent than PPIs, good for maintenance
Antibiotic Therapy
H. pylori Eradication Regimens
Triple Therapy (14 days)
- • PPI BID
- • Amoxicillin 1g BID
- • Clarithromycin 500mg BID
- • PPI BID
- • Metronidazole 500mg BID
- • Clarithromycin 500mg BID
Quadruple Therapy (14 days)
- • PPI BID
- • Bismuth subsalicylate 525mg QID
- • Tetracycline 500mg QID
- • Metronidazole 500mg TID
- Days 1-5: PPI + Amoxicillin
- Days 6-10: PPI + Clarithromycin + Metronidazole
Treatment Monitoring
Follow-up Testing
- • Test for cure 4-6 weeks post-treatment
- • Urea breath test preferred
- • Stool antigen test alternative
- • Avoid PPIs 2 weeks before testing
Symptom Resolution
- • Pain relief within 1-2 weeks
- • Complete healing 4-8 weeks
- • Endoscopy if refractory
- • Consider complications
Treatment Failure
- • Antibiotic resistance
- • Poor compliance
- • Alternative regimen needed
- • Culture and sensitivity
Nursing Interventions
Nursing Assessment
Subjective Assessment
- • Pain Assessment: Location, intensity (0-10 scale), character, timing
- • Associated Symptoms: Nausea, vomiting, bloating, heartburn
- • Dietary History: Food triggers, eating patterns, appetite changes
- • Medication History: NSAID use, prescriptions, OTC medications
- • Lifestyle Factors: Smoking, alcohol, stress levels
- • Family History: Peptic ulcer disease, H. pylori infection
Objective Assessment
- • Vital Signs: Blood pressure, heart rate, temperature
- • Abdominal Exam: Inspection, auscultation, palpation
- • Signs of Bleeding: Pallor, tachycardia, hypotension
- • Nutritional Status: Weight, BMI, signs of malnutrition
- • Stool Assessment: Color, consistency, occult blood
- • Skin Assessment: Color, temperature, capillary refill
Priority Nursing Diagnoses
Primary Nursing Diagnoses
- 1. Acute Pain related to gastric mucosal irritation
- 2. Risk for Bleeding related to ulcer erosion
- 3. Imbalanced Nutrition less than body requirements
- 4. Deficient Knowledge regarding disease management
- 5. Anxiety related to symptoms and diagnosis
- 6. Ineffective Health Maintenance related to lifestyle factors
- 7. Risk for Infection related to H. pylori
- 8. Nausea related to gastric irritation
Nursing Interventions by Category
Pain Management
- • Assess pain using standardized scale (0-10)
- • Administer prescribed medications as ordered
- • Monitor effectiveness of pain interventions
- • Encourage relaxation techniques
- • Position patient for comfort
- • Apply heat therapy if appropriate
- • Document pain assessments and interventions
- • Avoid NSAIDs and aspirin
Bleeding Prevention & Monitoring
- • Monitor vital signs every 4 hours
- • Assess stool for occult blood
- • Monitor hemoglobin and hematocrit levels
- • Observe for signs of bleeding (hematemesis, melena)
- • Maintain IV access if indicated
- • Educate patient on bleeding warning signs
- • Prepare for emergency interventions if needed
- • Document all findings accurately
Patient Education
Teaching Points
Medication Education
- • Take medications as prescribed
- • Complete entire antibiotic course
- • Take PPIs 30 minutes before meals
- • Avoid NSAIDs and aspirin
- • Report side effects promptly
- • Don’t skip doses
Dietary Modifications
- • Eat small, frequent meals
- • Avoid trigger foods
- • Limit caffeine and alcohol
- • Include high-fiber foods
- • Stay hydrated
- • Eat slowly and chew thoroughly
Lifestyle Changes
- • Smoking cessation
- • Stress management techniques
- • Regular exercise routine
- • Adequate sleep
- • Hand hygiene practices
- • Follow-up appointments
Emergency Interventions
Signs Requiring Immediate Action
- • Hematemesis or coffee-ground vomiting
- • Black, tarry stools (melena)
- • Severe abdominal pain
- • Signs of shock (hypotension, tachycardia)
- • Rigid, board-like abdomen
- • Severe nausea and vomiting
Immediate Nursing Actions
- • Notify physician immediately
- • Establish large-bore IV access
- • Monitor vital signs closely
- • Keep patient NPO
- • Position patient comfortably
- • Prepare for possible endoscopy
Complications
Gastrointestinal Bleeding
Incidence:
15-20% of peptic ulcer patients
Types:
- • Acute bleeding: Hematemesis, melena
- • Chronic bleeding: Iron deficiency anemia
- • Occult bleeding: Positive FOBT
Management:
- • IV fluid resuscitation
- • Blood transfusion if needed
- • Urgent endoscopy
- • PPI therapy
Perforation
Incidence:
5-10% of peptic ulcer patients
Presentation:
- • Sudden, severe abdominal pain
- • Board-like abdominal rigidity
- • Signs of peritonitis
- • Free air on chest X-ray
Management:
- • Emergency surgical repair
- • IV antibiotics
- • Nasogastric decompression
- • Fluid resuscitation
Gastric Outlet Obstruction
Cause:
Scarring and fibrosis at pylorus
Symptoms:
- • Persistent vomiting
- • Early satiety
- • Weight loss
- • Succussion splash
Treatment:
- • Endoscopic balloon dilation
- • Surgical bypass
- • Nutritional support
Malignant Transformation
Risk:
Higher with gastric ulcers, H. pylori infection
Prevention:
- • H. pylori eradication
- • Regular endoscopic surveillance
- • Biopsy of gastric ulcers
- • Follow-up endoscopy
Warning Signs:
- • Non-healing ulcers
- • Progressive weight loss
- • New onset dyspepsia >55 years
Complication Risk Factors
Patient Factors
- • Age >65 years
- • Comorbid conditions
- • Previous complications
- • Poor nutritional status
- • Smoking history
Ulcer Characteristics
- • Large size (>2cm)
- • Deep penetration
- • Posterior duodenal location
- • Multiple ulcers
- • Refractory to treatment
Medication Factors
- • High-dose NSAID use
- • Anticoagulant therapy
- • Steroid use
- • Poor medication compliance
- • Drug interactions
Prevention Strategies
Primary Prevention
H. pylori Prevention
- • Good hygiene practices: Regular handwashing
- • Safe food handling: Proper cooking and storage
- • Clean water sources: Avoid contaminated water
- • Avoid sharing utensils: Personal eating implements
- • Sanitation improvements: Public health measures
- • Screen family members: If infected
NSAID-Related Prevention
- • Use lowest effective dose: Minimum duration
- • Consider alternatives: Acetaminophen, topical agents
- • COX-2 selective inhibitors: If NSAID needed
- • Co-prescribe PPIs: For high-risk patients
- • Regular monitoring: GI symptoms assessment
- • Patient education: Risk awareness
Lifestyle Modifications
Dietary Changes
- • Regular meal times
- • Smaller, frequent meals
- • Limit spicy, acidic foods
- • Reduce caffeine intake
- • Avoid alcohol excess
- • High-fiber diet
- • Adequate protein intake
Stress Management
- • Regular exercise routine
- • Relaxation techniques
- • Adequate sleep (7-9 hours)
- • Meditation or yoga
- • Counseling if needed
- • Work-life balance
- • Social support systems
Avoid Risk Factors
- • Smoking cessation
- • Limit alcohol consumption
- • Avoid unnecessary NSAIDs
- • Manage chronic conditions
- • Regular medical checkups
- • Medication compliance
- • Prompt treatment of symptoms
Secondary Prevention
High-Risk Patient Management
Prophylactic Strategies
- • PPI co-prescription with NSAIDs
- • H2 blocker alternatives
- • Misoprostol for high-risk patients
- • Regular GI assessment
- • Endoscopic surveillance
- • Laboratory monitoring
Risk Stratification
- • Age >65 years
- • History of peptic ulcer disease
- • Concurrent anticoagulation
- • High-dose or multiple NSAIDs
- • Comorbid conditions
- • H. pylori infection
Patient Education for Prevention
Key Teaching Points
- • Recognize early warning signs
- • Importance of medication compliance
- • Lifestyle modification benefits
- • When to seek medical attention
- • Proper medication use
- • Regular follow-up importance
Red Flag Symptoms to Report
- • Severe or worsening abdominal pain
- • Vomiting blood or coffee-ground material
- • Black, tarry stools
- • Unexplained weight loss
- • Persistent nausea/vomiting
- • Signs of anemia
Memory Aids & Mnemonics
ULCER Mnemonic
PAIN Assessment
Triple Therapy Memory Aid
RED FLAGS Mnemonic
Gastric vs Duodenal
Duodenal Characteristics
Forrest Classification
Visual Memory Aids
Stomach Clock Analogy
Think of the stomach as a clock face:
- • 12 o’clock: Fundus (top)
- • 3 o’clock: Greater curvature
- • 6 o’clock: Antrum (bottom)
- • 9 o’clock: Lesser curvature (common ulcer site)
Traffic Light System
Use colors to remember severity:
- • GREEN: Mild symptoms, outpatient care
- • YELLOW: Moderate, needs monitoring
- • RED: Severe complications, emergency
