Peptic Ulcer Disease
-Burning epigastric pain exacerbated by fasting and improved with meals
-both gastric and duodenal ulcers (breaks in mucosal surface with depth to the submucosa)
PUD Risk Factors
-Helicobacter pylori and NSAIDs are the most common risk factors for PUD
H PYLORI and NSAIDS
-Additional risk factors: chronic obstructive lung disease (2.34), chronic renal insufficiency, current tobacco use, former tobacco use, older age, three or more doctor visits in a year, coronary heart disease, former alcohol use, African-American race, obesity, and diabetes . The mechanisms by which some of these risk factors lead to ulcer disease
Cigarette smoking has been implicated in the pathogenesis of PUD. Not only have smokers been found to have ulcers more frequently than do nonsmokers, but smoking appears to decrease healing rates, impair response to therapy, and increase ulcer-related complications such as perforation
Epigastric pain described as a burning or gnawing discomfort can be present in both DU and GU. The discomfort is also described as an ill-defined, aching sensation or as hunger pain. The typical pain pattern in DU occurs 90 minutes to 3 hours after a meal and is frequently relieved by antacids or food. Pain that awakes the patient from sleep (between midnight and 3 A.M.) is the most discriminating symptom, with two-thirds of DU patients describing this complaint
-Penetration is a form of perforation in which the ulcer bed tunnels into an adjacent organ. DUs tend to penetrate posteriorly into the pancreas, leading to pancreatitis, whereas GUs tend to penetrate into the left hepatic lobe. Gastrocolic fistulas associated with GUs have also been described.
GASTRIC OUTLET OBSTRUCTION
-Barium studies of the proximal GI tract
-Test for Hpylori
-Endoscopy provides the most sensitive and specific approach for examining the upper GI tract
- Screening for aspirin or NSAIDs (blood or urine) may also be necessary in refractory H. pylori–negative PUD patients.
Three types of studies routinely used include serologic testing, the 13C- or 14C-urea breath test, and the fecal H. pylori (Hp) antigen test.
-eradication of H. pylori and therapy/prevention of NSAID-induced disease is the mainstay of treatment.
-Meds: H2 Receptor Antagonists
Four of these agents are presently available (cimetidine, ranitidine, famotidine, and nizatidine), and their
PPI Omeprazole, esomeprazole, lansoprazole, rabeprazole, and pantoprazole
-Combination therapy for 14 days provides the greatest efficacy
The combination of bismuth, metronidazole, and tetracycline was the first triple regimen found effective against H. pylori.
The agents used with the greatest frequency include amoxicillin, metronidazole, tetracycline, clarithromycin, and bismuth compounds.
Quadruple therapy (Table 348-4), where clarithromycin is substituted for metronidazole (or vice versa), should be the next step. IF triple therapy dint work
Gastric Ulcer Presentation
Pain NOT relieved by food, midline, left of midline
epigastric pain 1-3 hours after eating
Pian reliereved by anatacids or food
pain on palpation 1 inch or farther to the RIGHT of midline