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Peptic Ulcer Disease Gastric and Duodenal Ulceration

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Peptic Ulcer Disease Gastric and Duodenal Ulceration

Key Points

  • PUD involves erosions or ulcers in upper gastrointestinal mucosa, most commonly in the stomach or duodenum.
  • Leading causes are NSAID exposure and Helicobacter pylori infection.
  • Disease burden is increased by smoking, alcohol use, obesity, and socioeconomic barriers.
  • Nursing priorities are bleeding/perforation surveillance, trigger reduction, and adherence to acid-suppression and eradication strategies.

Pathophysiology

PUD reflects disruption of mucosal defenses against acid-peptic injury, resulting in focal erosion and ulcer formation. Although disease can involve multiple upper-GI sites, gastric and duodenal involvement is most common.

Common etiologies include H. pylori infection and medication-related mucosal injury, especially NSAID use; additional contributors can include severe physiologic stress, selected medications, and malignancy-related processes.

NSAID-associated disease is strongly linked to COX-1 inhibition and reduced prostaglandin-mediated mucosal protection. H. pylori-associated disease involves mucosal inflammation, impaired bicarbonate-mediated defense, and persistent epithelial injury that can increase malignant-transformation risk.

Classification

  • Gastric ulcer pattern: Ulceration in the stomach.
  • Duodenal ulcer pattern: Ulceration in the proximal small intestine.
  • Other-site pattern: Less common involvement of esophagus or jejunum.

Nursing Assessment

NCLEX Focus

Differentiate uncomplicated dyspeptic symptoms from bleeding or perforation cues requiring urgent escalation.

  • Assess symptom pattern, severity, and chronicity of upper-GI discomfort, including location-timing relationships.
  • Distinguish common pain timing patterns: gastric-ulcer pain often soon after meals, duodenal-ulcer pain often 2-3 hours after meals and possibly nocturnal.
  • Screen exposure risks, including NSAID use, smoking, alcohol use, and other ulcerogenic medications.
  • Identify social and behavioral factors that can limit treatment adherence or recurrence prevention.
  • Escalate for potential complication cues such as low red-cell indices, hematemesis, blood in stool, or unintended weight loss.
  • Differentiate ulcer-related pain from potential myocardial-ischemia presentations and escalate cardiac-rule-out workflows when clinically indicated.
  • Monitor vital-sign shifts, hemoglobin/hematocrit trends, and stool/emesis blood presence for active hemorrhage or perforation concern.

Diagnostics

  • EGD (gold standard): Directly visualizes ulcer lesions and supports biopsy-based evaluation, including H. pylori assessment.
  • Alternative imaging: Barium swallow may be used when EGD is not feasible.
  • Complication imaging: CT abdomen is considered when perforation or other acute complications are suspected.
  • Bleeding assessment: Stool occult-blood testing supports evaluation of covert GI bleeding.
  • Laboratory support: CBC helps assess anemia from bleeding; H. pylori evaluation can include blood, stool, urine, and urea-breath testing.

Nursing Interventions

  • Reinforce avoidance or modification of ulcerogenic exposures when clinically possible.
  • Support diagnostic confirmation and cause-directed treatment pathways.
  • Monitor for acute deterioration (for example bleeding or perforation progression) and escalate promptly.
  • Align care goals with rapid pain control, blood-free stool/emesis trends, cause-treatment understanding, and nutrition/weight recovery.
  • Prioritize lifestyle measures that reduce recurrence burden, including smoking cessation, alcohol/caffeine/spice moderation, and weight optimization.

Pharmacology

Drug ClassRole in PUD CareKey Nursing Considerations
PPIs and H2 blockersAcid suppression to relieve symptoms and promote ulcer healingLong-term PPI exposure requires periodic risk-benefit review (for example bone-health and cognitive-risk discussions as clinically appropriate).
H2 receptor antagonistsAdditional acid-reduction strategy in selected clientsVerify regimen adherence and symptom response trend.
mucosal-protective-therapyProstaglandin analog use (for example misoprostol) for NSAID-related risk reductionConsider when NSAID continuation is unavoidable and ulcer risk remains high.
antibioticsH. pylori eradication regimen component with PPIConfirm completion of full eradication course and follow-up testing plan.
  • When medication-triggered PUD is suspected, collaborate on deprescribing, dose reduction, or safer substitution of ulcerogenic agents when feasible.
  • Anticipate surgical consultation for refractory disease or major complications; procedures may include vagotomy or partial gastrectomy.
  • During inpatient care, support NG-tube management when ordered for decompression or complication management.
  • Teach strict NSAID/aspirin risk reduction, smoking cessation, and individualized dietary trigger avoidance (acidic/spicy/oily items and high-caffeine beverages).

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