PUD

Question 1

Epidemiology of PUD

Answer 1

• Lifetime prevalence 10%
• Incidence and prevalence decreasing due to recognition/Rx of H pylori, introduction of PPIs
• Highest cause of mortality: PUD bleeding

Question 2

Etiologies of PUD

Answer 2

• Erosion: destruction of mucosa that does not extend thru muscularis mucosa
• Ulcer: the destruction extends through and past muscularis mucosa
• Only gastric ulcers (not duodenal ulcers) have malignant potential
• 2 most common causes: NSAIDs and H Pylori
• Other causes: zollinger-ellison, maligancy, crown’s disease, viral infections, systemic diseases

Question 3

Clinical presentation of PUD

Answer 3

• Ab pain: intermittent epigastric pain 2-3 hrs post meal
• Relieved w/ food or antacids
• Poor sensitivity/specificity
• Bleeding ulcer Sx: hematemesis, melena, hematochezia (if fast bleed)
• High risk (continuous bleeding) vs low risk (clean base ulcer)
• High risk pts get endoscopic Rx and IV PPI, low risk pts get oral PPI
• Other complications: obstruction, perforation, pancreatitis (penetration)

Question 4

Gastric outlet obstruction

Answer 4

• Pyloric ulceration leads to inflammation and scarring
• Sx: postprandial N/V
• PE: succussion splash (palpation), large gastric volume

Question 5

Pathophysiology of PUD

Answer 5

• Imbalance of aggressive and defensive factors
• Aggressive factors: HCl (parietal cell), histamine (ECL), pepsin (chief cell), gastrin (G cell), ACh from vagus
• Defensive factors: bicarb, mucus layer, epithelium and stem cells, mucosal blood flow

Question 6

H Pylori and PUD

Answer 6

• Found in the majority of PUD pts
• H Pylori causes damage to mucosa in 3 ways:
• Production of local toxic substances (urease, breaks down the unstirred layer and creates ammonia)
• Causes mucosal immune response (IL8 and recruitment of inflammatory cells)
• Increases gastrin and gastric acid secretion (due to decrease in antral somatostatin)
• H Pylori is associated w/ gastric adenoCA and low-grade B cell lymphoma of MALT
• Ulcer formation is primarily immunopathogenic

Question 7

H Pylori Dx

Answer 7

• Invasive (rapid urease assay, histology, and culture) requires endoscopy and biopsy
• Non-invasive: serology, stool Ag, carbon-labeled urea breath test
• Serology only good for populations w/ high H pylori incidence

Question 8

H Pylori Rx

Answer 8

• Either triple therapy or quadruple therapy (where clarithromycin resistance rates are >15-20%)
• Tripple Rx: amoxicillin, clarithromycin, PPI
• Quadruple Rx: metronidazole, bismuth subsalicylate, tetracycline, PPI
• After Rx must F/U pt w/ stool Ag or urea breath test

Question 9

NSAIDs and PUD

Answer 9

• NSAIDs contribute to mucosal damage thru a number of ways:
• Direct epithelial injury
• Inhibition of COX-mediated (mostly COX1) PG synthesis: this increases acid secretion, but most importantly decreases mucosal blood flow
• Microvascular injury: increases PMN adherence
• Most important cause of PUD from NSAIDs is inhibitin COX-mediated PG synthesis, which leads to decreased mucosal blood flow and increased WBC adherence

Question 10

Strategies for reducing NSAID related PUD

Answer 10

• Use non-NSAID analgesic (tylenol)
• Lower dose of NSAID (even low dose ASA contributes to PUD)
• Administer anti-acid co-Rx (PPI, misoprostol, sucralfate)
• Use les injurious NSAID (COX2 inhibitors) if low CV risk
• COX2 inhibitors allow for PG synthesis by COX1 in the GI mucosa
• However COX2 inhibitors have increased risk of CVD, due to not inhibiting COX-1 synthesis of TxA2 and thus promoting platelet activation/aggregation
• Traditional NSAIDs may also carry a similar risk

Question 11

Goals of PUD Rx

Answer 11

• Relieve Sx and heal ulcers accomplished by acid suppression (PPI)
• Prevent ulcer recurrence accomplished by Rxing the underlying disease (NSAIDs or H Pylori)
• Rxing H Pylori: tripple or quadruple therapy based on clarithromycin resistance rates
• Rx of NSAIDs: if they need to be used then use COX2 inh or add PPI/misoprostol (PG analog)/sucralfate (mucosal coating)