PUD Flashcards
1
Q
Epidemiology of PUD
A
- Lifetime prevalence 10%
- Incidence and prevalence decreasing due to recognition/Rx of H pylori, introduction of PPIs
- Highest cause of mortality: PUD bleeding
2
Q
Etiologies of PUD
A
- 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
3
Q
Clinical presentation of PUD
A
- 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)
4
Q
Gastric outlet obstruction
A
- Pyloric ulceration leads to inflammation and scarring
- Sx: postprandial N/V
- PE: succussion splash (palpation), large gastric volume
5
Q
Pathophysiology of PUD
A
- 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
6
Q
H Pylori and PUD
A
- 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
7
Q
H Pylori Dx
A
- 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
8
Q
H Pylori Rx
A
- 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
9
Q
NSAIDs and PUD
A
- 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
10
Q
Strategies for reducing NSAID related PUD
A
- 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
11
Q
Goals of PUD Rx
A
- 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)