Post on 07-May-2015
Peptic Ulcer Disease
Andrea M. Wilkins-Daly
BSc.,PharmD October 2009
Peptic Ulcer Disease
• Peptic Ulcer - an imbalance between aggressive factors (gastric acid and pepsin) +protective factors (gastric mucus, bicarbonate, prostaglandins).
• Peptic ulcers are chronic most often solitary, lesions that occur in any portion of gastrointestinal tract exposed to the aggressive action of acid-peptic juices.
Pathophysiology
Duodenal Ulcer – H.pyloric (95%)
- NSAIDS
Gastric Ulcer – NSAIDS
H.pyloric
ROLE OF H. Pylori INFECTION
H. pylori infection is present in almost all patients with duodenal ulcers and 70% cases with gastric ulcers.
Duodenal ulcers - Usually associated with gastritis confined to the antrum.
Gastric ulcers - Usually associated with pangastritis (inflammation of the entire stomach)
.
Other factors causing PUD -high gastrin level and excess acid production. Gastrinoma may
cause multiple peptic ulceration as in Zollinger Ellison syndrome. There is increased parietal cell mass.
- impaired mucosal defense . The gastric acid and pepsin levels are normal and no H.pylori are present.
- Chronic use of NSAIDs (aspirin) causes suppression of mucosal prostaglandin and direct irritative topical effect.
• Repeated use of corticosteroid and Chemotherapy in high dose.
• Cigarette smoking impair healing and favour recurrences.
• Alcoholic cirrhosis.• Psychological stress, ischemia.
Sites of Peptic Ulcer
• Duodenum: First portion ( few cms from the pyloric ring). Anterior wall is more often affected.
• Stomach: Usually antrum. Lesser curvature (common) . Anterior and posterior wall and greater curvature (less common).
• In the margins of a gastroenterostomy (stomal ulcer)• In the duodenum, stomach or jejunum of patients with
Zollinger-Ellison syndrome.
Mechanism of H pyloric
• Mechanism – H pylori secretes urease (generates ammonia), protease (breaks down glycoprotein in the gastric mucus)
• - breakdown of mucosal defense
****Show H plyoric Slide**treatment options
H
Mechanism Of H pyloric
• Damage of the protective mucosal layer. The epithelial cells are exposed to the damaging effect of acid-peptic digestion.
• Inflammation of the gastric mucosa.
• Chronically inflamed mucosa more susceptible to acid- peptic injury and prone to peptic ulceration.
• Ulcers occur at sites of chronic inflammation Eg - Antrum
PEPTIC ULCER DISEASE
Duodenal Ulcer
Duodenal Ulcer
DU in 65yo male
DU in 35 yo female
Duodenal ulcer
Pathophysiology
Case Presentation
• Mr. Sloley is a 45 year old male who
presents to your clinic with epigastric
abdominal pain x 2 weeks.
• What is your initial differential diagnosis at this point given the limited information?
Case Presentation
Mr Sloley History • PMH: HTN stable, Osteoarthritis in knees,
treated for an ulcer 3 years ago • Meds: Hydrochlorothiazide, ibuprofen prn • Soc HX: Married, employed as bank manager,
smokes 1ppd x 20years, drinks 2 beers per day, and 2-4 cups coffee per day
• What risk factors can you identify for PUD?
Diagnosis of H pyloric
• Breath Tests & Stool antigen tests
- Urea Breath Test ( 95-100% specificity)
-In office test (breath)
• Urea Blood test – Less Specific
• Endoscopy – culture of organism to determine antibiotic therapy
• Serologic test – not reliable (persisting antibiodies)
PUD Diagnosis
Initial Differential Diagnosis More Common: • Gastroesophageal reflux disease • Nonulcer dyspepsia/ Gastritis • Ulcer disease • Gastroenteritis • Biliary colic or cholecystitis • Pancreatitis • Irritable bowel disease
Case Study
• Mr. Sloley is a 45 year old male who presents to your clinic with epigastric abdominal pain x 2 weeks. He describes it as a burning pain which is non-radiating and is worse after he eats. He has frequent belching with bloating sensation but denies nausea, vomiting, diarrhea, constipation, or weight loss. He has tried Maalox which do help a little.
• Which symptoms support the possible diagnosis of PUD?
Case Presentation
Signs and Symptoms of PUD • Epigastric pain is most common symptom • Pain described as gnawing, burning or annoying• May radiate to the back (consider penetration) • Pain occurs when stomach is empty• Relieved by food, antacids (duodenal),
Dyspepsia including belching/ bloating • Hematemesis or melena with GI bleeding
Gastric Ulcers
• Pts with Gastric or Duodenal ulcers have similar symptoms
• Lacks pattern
• Pain occurs at anytime of day: frequently immediately or within 1-3 hrs after a meal
• Mortality rate is higher in these patients
• 10% of pts with PUD present with complications and have no prior Hx of pain
Treatment Goals
• Relieve symptoms
• Healing of ulcer
• Eliminating cause of ulcer
Treatment
• No single medication works to get rid of H pylori infection.
• 2 combinations are available Triple or Dual Therapy
• Ideal treatment regimen for H pyloric has not been identified
Treatment Options
• PPI* + clarithromycin (500 mg bid) + amoxicillin (1 gm bid ) x 10-14 days
• Eradication rate 70-85%
• PPI* + clarithromycin (500 mg bid) + metronidazole (500 mg bid) x 10-14 days Eradication rate 70-85%, use with penicillin allergy
Treatment Options
• Bismuth subsalicylate 525 mg qid + metronidazole 250 mg qid), tetracycline (500 mg bid), ranitidine 150 mg bid or PPI* x 10-14 days
• Eradication rate 75-90%, use with penicillin allergy
Treatment Options
• PPI* + amoxicillin (1 gm bid) x 5 days, then PPI + clarithromycin 500 mg bid + tinidazole 500 mg bid x 5 days
• Eradication rates > 90%, efficacy shown only in European studies
Treatment Options
FDA approved regimens
Bismuth 525 mg qid + metronidazole 250 qid, tetracycline 500 mg qid x 2 weeks + H2RA x 4 weeks
Lansoprazole* 30 mg bid + clari 500 mg bid + amoxicillin 1 gm bid x 10 days
*Substitute omeprazole 20 mg bid x 10 d or esomeprazole 40 mg qd x 10d or rabeprazole 20 mg bid x 7 days
Treatment
H. Pylori Triple Therapy Treatment • Triple therapy for 14 days is treatment of choice • Two forms of triple therapy: PPI–based and
bismuth-based • PPI based = PPI + 2 antibiotics for 2 wk, cont
PPI for additional 2 weeks. • Bismuth-based = bismuth subsalicylate and 2
antibiotics, for 2 weeks with addition of H2- blocker to optimize ulcer healing.
Treatment
For NDAID-related PUD – removal of offending agent
- Use of an anti-secretory agent therapy for relieve of symptoms
- If H pyloric present- eradication therapy
- Prevention of PUD – H2RA or PPI or misprostol with pt with chronic NSAID use at risk for developing PUD
Treatment
• Patient Counseling – adherence to therapy, proper dosing, side-effects
• Surgery –reserved pts with refractory ulcers or hemorrhage
NEW DEVOLPMENTS
• Supplementation with vitamin C enhances the success of Helicobacter pylori eradication efforts, researchers from Iran report.
• **PLEASE REMEMBER TO READ CPT MANUAL ON DRUGS AND S/E