Gastric Ulcer vs Duodenal Ulcer

1. Incidence & Demographics

• Bailey & Love's, p. 8726-8727: "Duodenal ulcers are more common than gastric ulcers"

2. Location

3. Acid Secretion

• Sabiston, p. 1779: "patients with gastric ulcers caused by H. pylori can have normal or reduced total gastric acid production. Gastric ulcer formation is more likely caused by an inflammatory response to the bacterial infection itself."
• Bailey & Love's: "Patients with gastric ulceration have relatively normal levels of gastric acid secretion" vs duodenal/prepyloric ulcers where "gastric acid levels are higher."

4. Pain - The Classic Clinical Distinction

• S Das Manual of Clinical Surgery: "The pain appears immediately after taking food, so the patient becomes afraid of it but appetite remains good (cf. duodenal ulcer)... the patient may lose a little weight."
• S Das: "[Duodenal ulcer] pain appears 2.5 to 4 hours after meal when the stomach becomes empty, i.e. 'hunger pain'... Relief is obtained by taking food."

5. Vomiting

6. Haemorrhage (Bleeding)

7. Risk of Malignancy

• Gastric ulcer: Can be malignant (gastric carcinoma can ulcerate and mimic a benign ulcer). All gastric ulcers must be biopsied and followed up to confirm healing. Endoscopy with multiple biopsies is mandatory.
• Duodenal ulcer: Malignancy is extremely rare. A duodenal ulcer is almost always benign and does not require routine biopsy.
• Sabiston: "The significant difference is the possibility of malignancy in a gastric ulcer. This critical difference necessitates that cancer be ruled out in acute and chronic presentations of gastric ulcer disease."
• Bailey & Love's: "Gastric ulcers may be malignant and an ulcerated gastric cancer may mimic a benign ulcer."

8. Complications

9. H. pylori Association

• In duodenal ulcer: H. pylori causes hypergastrinemia and increased acid secretion, which overwhelms the duodenal mucosa.
• In gastric ulcer: H. pylori causes chronic active gastritis with mucosal barrier disruption; acid levels may be normal. NSAID-induced ulcers occur more often in the stomach than the duodenum.

10. Treatment Principles

• Proton pump inhibitors (PPIs)
• H. pylori eradication (if positive)
• Cessation of NSAIDs/aspirin

Quick Summary Table

Stress Ulcer

Definition

"Stress ulceration is defined as an upper GI tract ulcer occurring because of hospitalization and most commonly occurs in the stomach." - Sabiston Textbook of Surgery

Pathophysiology

• Sabiston: "When stress is present, mucosal ischemia is thought to be the main factor responsible for the breakdown of these normal defense mechanisms."
• Harrison's 22e: "mucosal ischemia, breakdown of the normal protective barriers of the stomach, systemic release of cytokines, poor GI motility, and oxidative stress also play an important role." Notably, "Histologically, stress injury does not contain inflammation or H. pylori; thus 'gastritis' is a misnomer."

Named Eponymous Variants

• Schwartz's Surgery: "In 1842, Curling described duodenal ulcer and/or duodenitis in burn patients. Decades later, Cushing described the appearance of acute peptic ulceration in patients with head trauma (Cushing's ulcer)."
• Cushing's ulcer is the exception where acid secretion is actually elevated (vagally driven) rather than normal/low as in other stress ulcers.

Risk Factors for Clinically Significant Bleeding

1. Mechanical ventilation >48 hours (OR 15.6)
2. Coagulopathy (platelets <50,000/mm³; INR >1.5; PTT >2× normal) (OR 4.3)

• Respiratory failure
• Sepsis
• Hypotension / shock
• Hepatic failure
• Renal failure
• Corticosteroid use
• Injury Severity Score >16
• Spinal cord injury
• Age >55 years
• Emergency surgery, reoperation

"ICU admission by itself does not place patients at risk for hemorrhage... patients without these two risk factors have an overall risk of hemorrhage of only 0.1%, while those with both demonstrate clinically significant bleeding in 3.7%." - Maingot's

Morphology and Location

• Lesions are multiple, shallow (superficial), non-penetrating erosions - not true deep ulcers initially
• Located in the fundus and body (acid-secreting portion) of the stomach; rarely in the antrum; only rare duodenal lesions (except Curling's and Cushing's)
• Appear within hours of the insult (endoscopically detectable within 12-24 hours in >75% of patients)
• Early lesions: discrete erythema, focal hemorrhage, friability
• Histologically: coagulation necrosis of superficial epithelium + leukocyte infiltration of lamina propria; no fibrosis or scarring (unlike chronic peptic ulcers)
• As the lesion erodes into the submucosa, significant hemorrhage can occur

Clinical Presentation

• Usually painless - the patient may not have typical ulcer pain due to concurrent illness, sedation, or analgesics
• Presentation is almost always GI bleeding:
  • Overt: hematemesis, melena, frank blood in nasogastric tube aspirate
  • Occult: anemia, drop in hemoglobin
• Bleeding is usually slow and intermittent
• Clinically significant (hemodynamically compromising) bleeding occurs in only 0.5-5% of critically ill patients, despite endoscopic erosions being present in up to 90% after severe trauma

Incidence

• Endoscopic erosions: up to 90% after severe trauma/hypotension
• Clinically significant bleeding requiring transfusion/intervention: 0.5-5% (with improved ICU care, now closer to <5%, down from 20-30% historically)
• Mortality when hemodynamically significant stress ulcer bleeding occurs: >40%

Diagnosis

• Upper GI endoscopy is the gold standard
• Barium contrast studies are contraindicated (interfere with endoscopy and provide no useful information)
• Diagnosis must be distinguished from other causes of post-op bleeding (duodenal ulcer, gastric ulcer, esophagitis, varices)

Prophylaxis

• Gastric/duodenal bacterial overgrowth
• Aspiration pneumonia
• Clostridioides difficile infection

Treatment of Active Bleeding

1. Endoscopy - first-line (injection, cautery, clips)
2. Intra-arterial vasopressin or embolization (interventional radiology)
3. Surgery (last resort) - vagotomy + antrectomy, or total gastrectomy (extremely high mortality in critically ill patients)

Stress Ulcer vs Peptic Ulcer - Key Differences

Peptic Ulcer Disease and Psychological Stress

The Short Answer

Historical Context

• In 1940-1941, ulcer complications surged during the bombing of London (the Blitz) - one of the first documented links between catastrophic psychological stress and peptic ulceration
• After the 1995 Hanshin-Awaji earthquake in Japan, the incidence of gastric ulcers (particularly bleeding ulcers in older patients) rose significantly relative to duodenal ulcers
• The ancient connection between stress and ulcers was recognized long before H. pylori was discovered in 1982

"Ulcer complications are increased during catastrophic events, first demonstrated during the bombing of London during the Blitz in 1940 and 1941." - Yamada's Textbook of Gastroenterology 7e

Current Evidence: Is the Relationship Real?

• Two large population-based studies (a prospective Danish cohort and a US cross-sectional study) both found by multivariate analysis that mental health problems - severe stress, depressed mood, suicidal ideation, and psychological counseling - were independently associated with higher prevalence of PUD
• Prospective studies show increased risk of ulcer occurrence and recurrence in cohorts with:
  • Adverse life events
  • Chronic psychological stress
  • Anxiety and depressive symptoms
  • Social problems
  • Post-traumatic stress disorder (PTSD)
• Kaplan & Sadock's Comprehensive Textbook of Psychiatry references a Clinical Gastroenterology and Hepatology (2015) study confirming: "Psychological stress increases risk for peptic ulcer, regardless of Helicobacter pylori infection or use of NSAIDs"

• Overall quality of evidence is not high - ethical and logistic constraints limit study design
• Many older studies failed to control for H. pylori status, NSAID use, and smoking
• PUD is associated with personality traits (e.g., neuroticism), but neuroticism is also seen in non-ulcer dyspepsia and other functional disorders - making it non-specific
• Causality is difficult to establish

"It does appear that there is an independent relationship between psychological factors and the risk of developing PUD." - Yamada's Textbook of Gastroenterology 7e

"Psychological stress has been thought to contribute to PUD, but studies examining the role of psychological factors in its pathogenesis have generated conflicting results." - Harrison's Principles of Internal Medicine 22e

Proposed Mechanisms

1. Direct Biological Mechanisms

2. Indirect Behavioral Mechanisms

• Smoking - increases acid, reduces bicarbonate, impairs H. pylori clearance
• Alcohol use - direct mucosal irritant
• NSAID/aspirin use - stress-related pain management
• Poor diet and irregular meals - disrupts normal gastric acid regulation
• Sleep deprivation - reduces mucosal repair
• Reduced adherence to H. pylori eradication therapy

Stress as a Cofactor, Not a Standalone Cause

"Although PUD is associated with certain personality traits (neuroticism), these same traits are also present in individuals with nonulcer dyspepsia and other functional and organic disorders." - Harrison's 22e

Psychological Stress vs Physiological Stress (Stress Ulcer) - A Clarification

Clinical Implications

1. Always test for H. pylori - even in patients whose ulcer seems "stress-related"; stress may simply have unmasked a pre-existing H. pylori infection
2. Address behavioral risk factors - smoking cessation, limiting alcohol and NSAIDs
3. Psychiatric comorbidity - in patients with PTSD, depression, or anxiety with recurrent ulcers, treat both conditions concurrently
4. Psychosocial assessment is part of holistic ulcer management, particularly in cases of recurrent or treatment-resistant PUD
5. Stress management, cognitive behavioral therapy, and social support may reduce ulcer recurrence as adjunctive measures alongside standard PPI / H. pylori eradication therapy

Summary