18 peptic ulcer
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Peptic ulcer
Chen Jie
Department of gastroenterology, The first affiliated hospital of Sun Yat-sen university
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Ulcer
Erosion
Definition
Chronic ulcer occur in stomach and duodenum(Pathologically, ulcer is a lesion extending deeper into submucosa)
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•Epidemiology A common disease in digestive system
No data are available about the exact incidence of peptic ulcer
worldwide
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CO2 +H2O HCO3 HCO3
HCO3 HCO3
pH 2pH 3pH 4pH 5pH 6pH 7
H+ H+ H+ H+
Mucus
Bicarbonate
Epithelial cell
Bllod flow
Capillary
Artery of submucosa
Gastral cavity
Ideograph of gastric mucosa barrier
PGE (prostaglandin e)
EGF(epidermal growth factor)
Gastric acid and pepsin
Pathogenesis
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Pathogenesis
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Helicobacter pylori, Hp(transmission electron microscope )
Hp is an important etiological factor of peptic ulcer
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Evidences
Detection rate of Hp in PU patients1
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Recurence rate of PU after successful eradication of Hp
2
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Cyclo-oxygenase (COX)(rate-limiting enzyme in PG synthesis)
Arachidonic acid
COX-1Tissue type
COX-2Induced type
NSAIDsProstaglandin
NSAIDs(non-steroidal anti-inflammatory drugs) is another important etiological factor of PU
(-)
(-)
Prostaglandin
Gastrointestinal tract
Physiological function
Inflammation
Inflammatory reaction
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“No acid, no ulcer” --- Key role of gastric acid in the formation of peptic ulcer
Because the activation of pepsin is pH-dependent (pH<4)
Gastric acid and pepsin
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Diagnosis and differential diagnosis
Symptom is the most important clue for clinical diagnosis
Typical upper abdominal pain: Chronic, periodic and rhythmical pain
Relieve after food eating or antacid using
(Attention: Symptomless or un-typical ulcer)
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Complex ulcer: --ulcers occur in both gastric and duodenal mucosa Ulcer of pyloric canal: --usually cause pyloric obstruction
Postbulbar ulcer Macrosis ulcer: --size>2cm
Peptic ulcer in elderly people Symptomless ulcer --half of the NSAIDS-related ulcers are symptomless
Special type of peptic ulcer
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Definite diagnosis of peptic ulcer depends on endoscopy examination:
--- may observe ulcer, take biopsy and
detect HP infection
Niche sign observed by X-ray barium meal examination may also provide evidence for definite diagnosis of peptic ulcer
---not as accurate as endoscopy detection
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Pictures of PU under endoscopy
DU GU
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X-ray barium meal examination --- Niche sign (direct sign of ulcer)
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Virulence (biopsy specimen of gastric mucosa)
Histological examination Hp culture Rapid urease test
Non-virulence 13C or 14C urea breath test Hp antigen detection in stool Serologic examination of Hp antibody
Hp detection (routine)
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Steiner silver stain of gastric mucosa, showing abundantly microorganisms scattered within mucus (dark arrow indicated)
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Culture
Very small and translucent colony on the plate
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Rapid Urease Test: urea in the reagent was broken down by Hp urease, then the PH value of the reagent changed, finally the yellow color of the reagent changed to read color
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13C Urea Breath Test
(UBT)
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Differential diagnosis Peptic ulcer need to be differentiated from
diseases with chronic upper abdominal pain Diseases of liver, gallbladder and pancreas, functional
dyspepsia
After the ulcer has been detected by endoscopy examination
The differential diagnosis of benign and malignant gastric ulcer is very important
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---larger size, dirty moss, swollen and stiff surrounding mucosa---cancer--- Definite diagnosis must depend on biopsy and pathohistological examination!!
Gatric ulcer Gatric cancer
Benign and malignant gastric ulcer
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Complications
Bleeding The most common complication The most common cause of massive hemorrhage o
f gastrointestinal tract Perforation Pyloric obstruction Canceration (GU, 1%)
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Pyloric obstruction (DU 、 pyloric canal ulcer)
Temporary obstruction (caused by pyloric dropsy or pylorospasm during the active stage of ulcer)
Chronic obstruction (cicatricial pyloric obstruction) (caused by shrink of scar during the healing stage of ulcer)
Symptoms (abdominal pain, nausea, vomit, et al)
Confirmed by gastroscope or X-ray barium meal examination
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TreatmentPrinciples
Eliminate etiological factors (Hp eradication, stop using NSAIDs)
Relieve symptoms, facilitate ulcer healing (antiulcer drugs)
Prevent ulcer recurrence, and prevent or treat complications
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1. General treatment
---Stop smoking, stop drinking ,regular food-intake, et al
2. Anti-ulcer treatment
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Types Commonly used drugs Recommend dosage
Acid inhibition drugs
Antacid Algeldrate, hydrotalcite et al
H2RA Cimetidine 800mg qN or 400mg bid
Ranitidine 300mg qN or 150mg bid
Famotidine 40mg qN or 20mg bid
PPI Omeprazole 20mg qd
Lansoprazole 30mg qd
Rabeprazole 10mg qd
Gastric mucosa protection drugs
Sucralfate Sucralfate 1g qid
Prostaglandins Misoprostol 200g qid
Bismuth compound Colloidal bismuth subcitrate 120mg qid
Anti-ulcer drugs
H2RA :Histamine H2 receptor antagonist; PPI :proton pump inhibitor
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3. Hp eradication treatment
Hp must be eradicated in all
Hp-positive peptic ulcer!!
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Proton pump inhibitor (PPI)
Two antibiotics
Colloidal Bismuth Subcitrate
Amoxicillin, Clarithromycin, Tetracycline, Metronidazole, Furaltadone…
+
(1) Hp eradication regimen
Or
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A trigeminy regimen of Hp eradication
Omeprazole 20mg b.i.d
+ Clarithromycin 500mg b.i.d
+ Amoxicillin 1000mg b.i.d
×
7days
This is a widely used first-line Hp eradication regimem.
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Ulcer patient with complications
Patient with large ulcer or recurrent ulcer
Symptom cannot be relieved after Hp
eradication
Above patients need to use PPI or H2RA for 2-
8weeks
(2)Anti-ulcer treatment after Hp eradication
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(3) Detect Hp after eradication treatment
4 weeks after eradication treatment
---- to avoid false negative result
13C or 14C-UBT is the first choice
Detect Hp infection by gastroscope is necessary in
DU patients with complications, or in GU patients
with or without complications
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4. Treatment and Prevention of NSAID-related ulcer
Treatment Stop using NSAIDs , routinely give H2RA or PPI for tre
atment
For patients who can not stop using NSAIDs, give PPI, an
d maintain long term anti-ulcer treatment after ulcer heal
ing
For patients with Hp infection , Hp eradication is also n
eeded
(NSAID and Hp are two independent ulcerogenic factors )
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Prevention
Following patients need routine prevention treatment:
Patients with a history of peptic ulcer Elderly patients Patients using glucocorticosteroid or decoagulant (inclu
ding low-dosage asprin) together with NSAIDs
Prevention method:PPI, routine dosage
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5. Prevention of peptic ulcer recurrence
2.Following patients need to maintain long term anti-ulcer treatment to prevent ulcer recurrence:
Patient who can not stop using NSAIDs
Hp can not be eradicated
Ulcer recurrence after Hp eradication
Non-Hp and non-NSAIDs ulcer Elderly patients Patients with serious concomitant disease
3. Prevention method: PPI or H2RA, routine dosage
1.Hp eradication and stop using NSAID may prevent peptic ulcer recurrence
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6. Indication for surgery
Hemorrhea, medical treatment is
ineffective
Acute perforation
Cicatricial pyloric obstruction Gastric ulcer with canceration
Telephium, medical treatment is
ineffective
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What is the etiopathogenisis of PU?
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How to diagnose PU?
Chronic, periodic and rhythmical upper abdominal pain
Endoscopy (or X-ray barium meal ) examination for definite diagnosis
Routinely detect Hp
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Common complications of PU?
• Bleeding
• Perforation
• Pyloric obstruction
• Canceration (GU, 1%)
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Case one: How to treat a young patient with DU, upper gastrointestinal bleeding and Hp infection?
Hp eradication (for example, PPI+Amo+Cla, 1w)
Continue to treat with anti-ulcer drug (for example, omep
razole 20mg qd, 2w)
Take endoscopy examination
4w after eradication, take 13C or 14C urea breath test
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Case two: How to treat a patient with gastric ulcer and Hp infection who needs to use NSAID for a long term?
Hp eradication (for example, PPI+Amo+Cla, 1w)
Continue to treat with PPI (for example, omeprazole 20mg
qd, 4w)
Take endoscopy examination
Continue long term maintenance treatment with PPI to pr
event recurrence (for example, omeprazole 20mg qd)
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Thank you!