Peptic Ulcer Disease

Question 1

• Disruption of the mucosa

- typically involves the proximal duodenum (90%) or the distal stomach (10%)

Answer 1

Peptic Ulcer Disease

Question 2

• Mucosa: Simple columnar epithelium with gastric glands; Lamina propria; muscularis mucosae
• Submucosa: Lymphatic, containing submucosal Meissner’s Plexus
• Muscularis: Circular and longitudinal layers of muscle, with Auerbach’s plexus in between
• Serosa: Peritoneal surface

Answer 2

Layers of the GI Tract

Question 3

necrotic mucosal defects that extend through the muscularis mucosae and into the submucosa

Answer 3

Ulcers

Question 4

superficial necrotic defects that spares the muscularis mucosae

Answer 4

Erosion

Question 5

Damaging forces:

• H. pylori (95% of duodenal ulcers; 75% Gastric ulcers)
• NSAIDS (can cause gastric ulcers)
• Bile reflux (can cause gastric ulcers)
• Aspirin
• Cigarettes
• Alcohol

Impaired defenses:

• Ischemia
• Shock
• Delayed gastric emptying

Answer 5

Etiology of PUD

Question 6

• Mucus Coat: Phospholipids form a hydrophobic layer
• Unstirred water layer rich in bicarbonate.
• Surface at pH 7 while lumen is pH 2

Answer 6

Mucosal Defense (Pre-epithelial)

Question 7

• Apical cell membranes
• Tight junctional complexes prevent acid pepsin inroads.
• Excess H+ Buffering with Na+/H+ and Cl-/HCO3- exchangers

Answer 7

Epithelial Defense Mechanisms

Question 8

• Blood flow - provides energy and substrate and removes acid that diffuses through the injured mucosa.
• “Alkaline Tide” - occurs in response to acid secretion of parietal cells.

Answer 8

Post-Epithelial Defense Mechanisms

Question 9

• Slow growing, highly motile, microaerophilic, gram negative, spiral bacteria
• infection results in cytokine release and inflammatory cascade: Lipopolysaccharide (lipid A Endotoxin); nap A gene (neutrophil-activating protein); Vacuolating Cytotoxin (VacA);
• Cytotoxin-Associated Antigen (Cag-A): more malignant with greater inflammation

Answer 9

H. pylori

Question 10

• IgG antibody titer by ELISA
• Agar gel slides: Antibiotics and PPI cause false negatives
• Membrane test
• Urea breath test
• Stool antigen HpSA

Answer 10

Tests for H. pylori

Question 11

Inhibit cyclooxygenase, thereby inhibiting Prostaglandins E2, I2 and F2alpha

• PGs protect the stomach and duodenum by increasing blood flow, bicarb production, and mucus production
• elderly more susceptible to ulcers from NSAID use
• gastric ulcers > duodenal ulcers

Answer 11

NSAIDs

Question 12

• Prior peptic ulcer disease.
• Prior NSAID complications
• Advanced age

Concomitant use of:

• glucocorticoids: does not cause ulcers alone
• Anticoagulants e.g. platelet aggregation inhibitors
• High doses of NSAIDS
• Comorbid diseases
• Ethanol use

Answer 12

Risk factors for NSAID-Induced Ulcers

Question 13

Nocturnal pain: usually around 2-3am

Alarm symptoms:

• Iron deficiency anemia
• Acute upper GI bleed in form of hematemesis
• Melena: black dotted, foul-smelling stools
• Pain radiating to back: ulcer might be penetrating to other organs like pancreas

Answer 13

Clinical presentation of PUD

Question 14

• Hemorrhage
• Perforation
• Penetration
• Obstruction

Answer 14

Complications of PUD

Question 15

• almost always due to H pylori
• Can be due to Zollinger Ellison Syndrome
• Presents with epigastric pain that improves with meals (b/c duodenum ramps up it’s defenses agaisnt acid)
• Bopsy shows hypertrophy of Brunner glands (glands w/in duodenum that produce mucus)
• May rupture, leading to bleeding from the gastroduodenal artery
• almost never malignant

Answer 15

Duodenal ulcer

Question 16

• presents with epigastric pain that worsens with meals
• Ulcer is usually located on the lesser curvature of the antrum
• rupture carries risk of bleeding from the left gastric artery
• can be caused by gastric carcinoma

Answer 16

Gastric ulcer