PEPTIC ULCER DISEASE
Peptic ulcer diseas-Tran Ngoc Anh MD
1.Recognize the typical clinical
presentation and risk factor for PUD
Objectives
2.Understand pathophysiology of
PUD focusing on HP
3.Describe an appropriate
PEPTIC ULCER DISEASE
diagnostic plan
4.Prescribe an appropriate
Peptic ulcer diseas-Tran Ngoc Anh MD
therapeutic regime
GENERAL CONSIDERATIONS
An ulcer: disruption of the mucosal integrity of the stomach and/or duodenum (surface >5mm in size, depth to the submucosa) Occur: Stomach
Chronic
Peptic ulcer diseas-Tran Ngoc Anh MD
and/or duodenum
ETIOLOGY and PATHOPHYSIOLOGY
Common Rare
Uncommon
• Helicobacter
• Crohn’s disease pylori infection
• Zollinger Ellison • Tumors (Cancer, lymphoma)
• Helicobacter helimannil • Idiopathic
• Viral infections • Radiation/che motherapy
• Vascular
• NAIS • Stress- related mucosal damage
insufficiency
Peptic ulcer diseas-Tran Ngoc Anh MD
ETIOLOGY and PATHOPHYSIOLOGY
CLINICAL FEATURES
1.Symptoms -Abdominal pain. 10%PU with a complication:
bleeding, perforation, obstruction
-Epigastric pain-Most common subtype: burning,
gnawing discomfort:
+DU: occurs 90 min to 3h after a meal; relieved by
Peptic ulcer diseas-Tran Ngoc Anh MD
antacids or food. Awakes from sleep +GU: discomfort precipitated by food -Nausea, Weight loss; more commonly in GU -Dyspepsia including belching, bloating
CLINICAL FEATURES
Common risk factor for gastric mucosa disruption:
Clinical pearls: NSAID: gastritis or ulcer silent. Ve
HP, NSAIDS/ASA(event at low dose), Coffe caffeine, Ethanol, Tobacco, Severe Physiology stress, Steroids
NSAIDS: 15%of patients longterm NSAIDS
Dyspeptic are non specific: 20-25%
Peptic ulcer diseas-Tran Ngoc Anh MD
(Piroxicam, Feldene, Ketorolac, Toraldo, Celceb, Indomethacine, Ibuprofen, Selective COX2)
CLINICAL FEATURES
2.Physical examination: few, non specific Epigastric tenderness (20% in right of the midline) Discovering evidence of ulcer complication Tachycardia, orthostasis: dehydration secondary to
vomiting, active gastrointestinal blood loss
Severely tender, Boardlike abdomen: perforation Succussion splash indicates retained fluid in the
Peptic ulcer diseas-Tran Ngoc Anh MD
stomach: gastric outlet obstruction
CLINICAL FEATURES
Typical symptoms
• Epigastric pain • Nausea • Fullness, Bloating • Early satiely • Nocturnal pain
• Anemia • Hematemesis, Melena,
Heme+ stool
Alarm symptoms
• Anorexia, weight los • Severe abdominal pain
Peptic ulcer diseas-Tran Ngoc Anh MD
LABORATORY FINDING
Radiographic-Barium study
Endoscopy
Others
Peptic ulcer diseas-Tran Ngoc Anh MD
LABORATORY FINDING
1.Barium studies -Older single contrast barium meals: 80% Double :90% -Not good in small ulcer -DU: Well demarcated crater in the bulb -GU: discrete with radiating mucosal folds
origanating from the ulcer margin
Peptic ulcer diseas-Tran Ngoc Anh MD
-Ulcer >3cm with mass: malignant
LABORATORY FINDING
LABORATORY FINDING
2.Endoscopy Most sensitive, specific Permet: direct visualization of the mucosa, tissue
biopsy-rule out malignancy, H.pylori
Peptic ulcer diseas-Tran Ngoc Anh MD
3.Others -CBC: acute/chronic blood loss -HP test
LABORATORY FINDING
LABORATORY FINDING
Se/Sp
Comments
Test
Invasive
Rapid urease
80-95/95-100 Simple, False (-) with PPI, Antibiotics,
Bismuth
Histology
80-90/.95
Require pathology processing and staining, provides histologic information
Culture
Time consuming, expensive, dependent on experience, allows determination of antibiotic susceptibility
Non invasive
Serology
>80/>90
Inexpensive, convenient, not useful for early follow up
>90/>90
Urea breath test
Simple, rapid; useful for early follow up, False (-) with PPI, Antibiotics, Bismuth
Stool antigen
>90/>90
Inexpensive, convenient; not establishd for eradication but promising
Peptic ulcer diseas-Tran Ngoc Anh MD
COMPLICATIONS
Perforation
Gastrointestinal bleeding
Gastric outlet obstruction
Peptic ulcer diseas-Tran Ngoc Anh MD
COMPLICATIONS
1. Gastrointestinal bleeding: Most common 15%, >60; Use NSAIDS Tarry stools, coffe ground emesis; 20% without any
preceding warning signs or symptoms
2.Perforation: Second most commonly 6-7%, elderly, NSAIDS Sudden onset of severe, generalized abdominal
pain
Penetration- -DU: Pancreas pancreatitis -GU: Left hepatic lobe
Peptic ulcer diseas-Tran Ngoc Anh MD
COMPLICATIONS
3.Gastric outlet obstruction The least common complication 1-2% patients Pain worsening with meal, nausea, vomiting of
Peptic ulcer diseas-Tran Ngoc Anh MD
undigested food. Weight loss
TREATMENT
• Acid
neutralizing/inhibitory drugs
INTERNAL MEDECINE
• Cytoprotective agents • Therapy of H.Pylori • Therapy of NSAID related gastric or duodenal
SURGICAL
• Fail of internal medecine • Complication
Peptic ulcer diseas-Tran Ngoc Anh MD
TREATMENT
Acid neutralizing/inhibitory drugs
H2 antagonists
Antacids
Proton Pump (H+K+ATPase)
• Use primarily in
• Mix . Aluminum, Mg hydroxide
• Maalox,
UD not associated with HP
Gastropulgite
• ↓gastric acid secretion by inhibiting the parietal cellH+K+ATPase
• Relieve pain, heal PU more rapidely than H2
• Inhibit the H2 receptor of parietal cell →reduced acid secretion(basal , stimulated)
• Before a meal • Duration 4w
• Once/day- bedtime
• Duration: 6-8w
Peptic ulcer diseas-Tran Ngoc Anh MD
Acid Suppressing Drugs
Drug type
Examples
Dose
Antacids
100-400mEq/l 1-3h after meals and hs
Mylanta, Maalox, P hosphalugel, Gastropulgie
H2 receptor antagonists
Cimetidine; Ranitidine; Famotidine; Nizatidine
400mg bid, 300mghs, 40mghs, 300mghs
Proton pump inhibitor
Omeprazole Lansoprazole Rebeprazole Pantoprazole Esomeprazole
20mg/d 30mg/d 20mg/d 40mg/d 20mg/d
Peptic ulcer diseas-Tran Ngoc Anh MD
Mucosal protective agents
Drug type Examples Dose
Sucralfate Misoprostol 1g qid 200 µg qid
Peptic ulcer diseas-Tran Ngoc Anh MD
Sucralfate Prostaglandin analogue Bismuth containing compounds Bismuth subsalicylat BBS
TREATMENT
Cytoprotective agents
Sucralfate
Prostaglandin analogue
Bismuth containing compounds
• Physicochemical
• The mechanism
is unclear: prevention of futher pepsin/HCl induced damage, HCO3, mucous secretion
• ↓Enhancement of mucosal defense, repair, Enhance mucous HCO3, stimulate mucosal blood flow, mucosal cell turnover
• 200 µg qid
barrier, promoting a trophic action, enhancing prostaglandin synthesis, stimulating mucous HCO3 secretion, enhancing mucosal defense, repair
• 1g quid
Peptic ulcer diseas-Tran Ngoc Anh MD
TREATMENT
PUD cause HP
PUD cause NSAID
Peptic ulcer diseas-Tran Ngoc Anh MD
Helicobacter pylori infection treatment regimens
Combination
TRIPLE THERAPY REGIMEN
LCA, OCA, PCA, RCA
Clarithromycin 500mg bid+ Amocicillin 1g bid or Metronidazole 500mg bid
Esomeprazole 20-40mg Lansoprazole 30mg po bid Omeprazole 20mg po bid Pantoprazole 40mg po bid Rabeprazole 20mg po bid
QUADRUPLE THERAPY REGIMEN
BMT-PPI or H2RA
Metronidazole 250mg qid +Tetracyclin 500mg po qid Bismuth 525mg po qid
1 of 5 PPI above or Cimetidine 300mg po qid Famotidine 20mg po bid Nizatidine 150mg po bid Ranitidine 150mg po bid
Peptic ulcer diseas-Tran Ngoc Anh MD
NSAID-Induced Ulcer Treatment Regimens
Treatment Option Drug use
Example
PPI
Discontinuation of NSAID
Dexlansoprazole 30- 60mg Esomeprazole 20-40mg Lansoprazole 15-30mg Omeprazole 20-40mg Pantorazole 40mg
H2RA
Cimetidin, Famotidine, Nizatidine, Ranitidine
Sucralfate 1g Same as PPI above
Prophylactic therapy
Mucosal protective agent PPI Selective COX2 inhibitor
Same as PPI above
PPI
Continuation of NSAID
H.P
Multiple
Peptic ulcer diseas-Tran Ngoc Anh MD
