1. Diagnosis and management of PUD
Ermias (MD)

2. History Abdominal pain (epigatric burn) Mechanism of pain
Common for DU, GU, NUD
10% present with complications with out antecedent pain, eg after NSAID
DU – 90min-3hr after meal, past midnight, - relieve with food, antacids
GU – worse with meal, nausea and weight loss are common
Mechanism of pain
Acid induced chemoreceptor activation in duodenum
Enhanced duodenal sensitivity to bile acids and pepsin
Altered gastro-duodenal motility

3. History conti… Alterations in pain may show complications
Persistent dyspepsia radiating to the back - penetrating ulcer to pancreas
Sudden onset severe generalized pain – peritonitis due to perforation (6-7%)
Worsening vomiting with meals – GOO (1-2%)
Tarry stool, coffee ground vomits - bleeding (15%)

4. Physical examination Epigastric tenderness
20 % slightly to the right of the mid line
In complications
Tachycardia, hypotension
Signs of peritonitis
Succussion splash

5. DDx NUD (functional, essential) Proximal GI tumors GERD
Pancreaticobiliary diseases
Crohn’s disease (gastro-duodenal)

6. diagnosis Empiric tx as NUD (<45 yrs age) Ba studies Endoscopy
Single contrast -80%, double contrast 90% sensitivity
See as well defined crater
Negative in <0.5cm ulcer, post op or scars
Endoscopy
Photography, tissue biopsy, source of blood loss, detection of small ulcers
H. pylori
Serum gastrin, gastric acid analysis - ZES

7. H. Pylori detections INVASIVE (ENDOSCOPY/BIOPSY REQUIRED) NON-INVASIVE
Rapid urease – (80–95/95–100) - Simple, false negative with recent use of PPIs, antibiotics, or bismuth compounds
Histology – (80–90/>95) - Requires pathology processing and staining;
Culture - Time-consuming, expensive, allows determination of antibiotic susceptibility
NON-INVASIVE
Serology – (>80/>90) - Inexpensive, convenient; not useful for early follow-up
Urea breath test – (>90/>90) - Simple, rapid; useful for early follow-up; false negatives with recent therapy
Stool antigen – (>90/>90) - Inexpensive, convenient; promising for eradication

8. treatment Schwartz – “no acid no ulcer” (old dictum) New concept
Eradication of H. pylori,
prevention of NSAID induced ds.

9. Acid neutralizing Antacids – symptomatic relief
Al(OH)3 Mg(OH)2
CaCO3, NaHCO3
H2 receptor blockers – for active ulcer tx with H pylori eradication (4-6wk)
Antiandrogenic, cyt P450 inhibitor,
Elevation of transaminases, cr, prolactin; pancytopenia
Proton pump inhibitors
Irreversibly inhibit H+K+ATPase
Rapid onset and prolonged half life
Hypergastrinemia, carcinoid tumors (in animals), hypochlorhydria (interfere with drug absorption)

10. Cytoprotective agents
Sucralfate
Complex sucrose salt of Al(OH)3 and sulfate
Forms viscous paste in the stomach
Gives physicochemical barrier from further tissue injury
Induce trophic effect on growth factors
Stimulate mucous and bicarbonate secretion
Enhance prostaglandin secretion
SE – constipation, neurotoxicity (Al) in renal failure

11. Bismuth preparations (colloidal bismuth subcitrate, subsalicylate)
Anti H pylori effect
Mech. for ulcer not clear
Prostaglandin analogues – misoprostal
Enhance mucous bicarbonate secretion, stimulate mucosal blood flow, decrease mucosal cell turn over
Se – diarrhea, uterine bleeding and contraction
200ug QID

12. Therapy of H pylori Dramatic decrease in ulcer recurrence GU 59% - 4%
DU 67% - 6%
Aim of initial eradication – 85-90%
Efficacy, pt tolerance, resistance pattern, cost
dual tx not recommended < 80% eradication
Unnecessary tx – drug resistance
Infection recurrence in 6 mnth is likely from recrudescence than reinfection

13. TRIPLE THERAPY
1.  Bismuth subsalicylate plus     Metronidazole plus     Tetracycline
2.  Ranitidine bismuth citrate plus     Tetracycline plus     Clarithromycin or metronidazole
3.  Omeprazole (lansoprazole) plus     Clarithromycin plus     Metronidazole or     Amoxicillin
QUADRUPLE THERAPY
Omeprazole (lansoprazole) Bismuth subsalicylate Metronidazole Tetracycline
2 tablets qid 250 mg qid 500 mg qid
400 mg bid 500 mg bid 500 mg bid
20 mg bid (30 mg bid) 250 or 500 mg bid 500 mg bid 1 gr bid
20 mg (30 mg) daily 2 tablets qid 250 mg qid 500 mg qid

14. Tx of NSAID related gastric injury
Stop the injurious agent
Use acid inhibitory agent (PPI, H2 blocker)
Prevention – misoprostol, PPI
Use of COX -2 inhibitors

15. Misoprostol PPI Selective COX-2 inhibitor
Recommendation
H2 blocker or PPI PPI
Misoprostol PPI Selective COX-2 inhibitor
Eradication if active ulcer or a past history of peptic ulcer disease
Clinical Setting
Active ulcer    
NSAID discontinued
NSAID continued
Prophylactic therapy
H. pylori infection

16. UGIE
4wk

17. GU vs DU GU (body, fundal) – likely to be malignant
Repeat endoscopy and biopsy at 8-12 wk
Non healing DU (8wk), GU (12wk) – refractory
Causes:
Poor compliance
NSAID use
Cigarette smoking
Malignancy
Gastric hyper secretary state (ZES)
Ischemia, Crohn’s ds, Amyloidosis, Sarcoidosis, Lymphoma, Eosinophilic gastroenteritis, CMV infection, Tuberculosis, syphilis

18. surgery Elective and emergency
Medically refractory ulcer and complicated ulcers (bleeding, perforation and GOO)
Surgical mx decreased with increased endoscopic interventions
Procedures:
1. vagotomy with drainage
2. highly selective vagotomy
3. vagotomy with antrectomy

20. complications Depend on the extent of anatomic modification
Complications of intra abdominal procedure
Recurrent ulcerations
Afferent loop syndrome
Dumping syndrome
Post vagotomy diarrhea
Bile reflux gastropathy
Maldigestions and malabsorption
Gastric adenocarcinoma