PEPTIC ULCER

Dr. Leonardo B Dairi, SpPD-KGEH

 PEPTIC ULCER

GASTRIC ULCER
DUODENAL ULCER
ESOPHAGEAL ULCER
Patient Problem:
Suffer recurrency / relaps, loss in the
works, cost of medication expensive
 EPIDEMOLOGY
Incidens in Western Countries:
Female 4 15 % & Male 10 15 %
Medan Jakarta
Peptic Ulcer 20,01 % 6,93 %

CA Gastro 5,18 % 1,73 %

Dispepsia Non Ulkus 72,15 % 88,4 %

Esofagitis 1,59 % 1,5 %

Common Causes of Death in U.S.
9

8
Death per 100,000

0
Leukemia AIDS NSAID-GI Melanoma Asthma Cervical
disease cancer

Wolfe et al. NEJM 1999

 DEFINITION
Peptic Ulcer: Damage of mucosal
layer/muscularis mucosa or deeper until
submucosa of the stomach/duodenum, ulcer
edge surounded by acute and chronic
inflamatory cells; the diameter 5 mm

Erosion: damage < 5 mm and the depth not

over than muscularis mucosa
 HISTORY / PATHOGENESE

1. NO ACID NO ULCER 1910 SCHWARTZ

2. DEFENSIVE FACTOR (nucus,mucosal

resistance,local mucosal blood flow)/AGGRESIVE
FACTOR(acid,pepsin)

3. NO HP NO ULCER WARREN AND MARSHALL

1983

GU : 60 80% HP, 25% OAINS, 5% ZES

DU : 90 - 95% HP, 5% OAINS, 5% ZES
 BALANCE THEORY SHAY
& SUN
Ulcer
Healing
Aggressive
Factor

Defensive
Factor BALANCE Acid
Shay & Sun
Pepsin
Mucus, mucin Food
Fosfolipida Alcohol
Ion bicarbonat NSAIDs
Prostaglandin
Mucous blood flow
Cell regeneration
 Differences between NSAID and
H.pylori induced ulcers
NSAIDs induced H.pylori
Patients Elderly more than Young more often
demographics young than elderly
Women more often Men more often than
than men woman
Site of damage Gastric more than Duodenal more than
duodenal gastric
Symptoms More often Usually pain and or
asymptomatic dyspepsia
Histology Surrounding mucosa Surrounding mucosa
normal inflammed
(foveolar hyperplasia) (active chronic
gastritis)

Scarpignato,1997
 Risk Factors for NSAIDs Induced
Gastroduodenal Ulceration

Established Possible

Advanced age Concomitant infection with

History of ulcer H. pylori
Concomitant use of glucocorticoids Cigarette smoking
High-dose NSAIDs Alcohol consumption
Multiple NSAIDs
Concomitant use of anticoagulants
Serious or multisystem disease
 H. pylori, NSAID use and risk of PUD:
a meta-analysis
Both H. pylori infection and NSAID use
independently and significantly increase the risk
of peptic ulcer and ulcer bleeding
H. pylori infection and NSAID use are
synergistic for peptic ulcer development and
ulcer bleeding

Huang et al., Lancet 2002; 359: 1422.

Hp increase risk of NSAID Ulcers
Meta-analysis of 16 studies consisting of 1633 patients

100 OR 3.55

80 OR 3.53 OR 19.4
HP+, NSAID+
60 OR 18.1 HP-, NSAID+
40 HP+, NSAID-
HP-, NSAID-
20

0
HP+, HP-, HP+, HP-,
NSAID+ NSAID+ NSAID- NSAID-

Huang et al. Lancet 2002

 Peptic Ulcer Clinical Manifestation
HISTORY OF ILLNESS
None
Dyspeptic Symptom:
Epigastric Pain, Nausea, Vomiting,anorexia,
epigastric discomfort, etc
Epigastric Pain
Episodic, Nocturnal, Pain-Food- Relief pattern
can be pointed at
Loss of body weight
Hematemesis and Melena
 DIAGNOSTIC
1. Simptom 25 % mild, 50 % moderate, 25 %
severe with/without complication.
Cardinal simptom epigastric pain or dyspepsia.
2. Physical Examination and Laboratory tests are
typically normal.
3. Radiology/OMDF (Crater-Niche -->TL)
4. Endoscopy : gold standard diagnostic peptic
ulcer
 Indication of Upper Gastrointestinal/
Esophago-gastro-duodenoscopy
Age over 45 years old
Alarm signs
Therapy failure
History of Peptic ulcer + Complication
Patient enquery
The use of aspirin or NSAID
Abnormality in Upper GI X-Ray (OMD)
 Diagnosis of
Helicobacter Pylori Infection
NON-INVASIVE INVASIVE
Urea Breath Test (biopsy & endoscopy)
Serum serology for Hp Culture test
antibody test Histopatology test
Whole blood serology for Urease test
Hp antibody test
PCR
Saliva Assay for Hp
antibody test
Helicobacter Pylori stool
antigent (HpSA) test
 MANAGEMENT
GENERAL/ SUPPORTIVE
SYMPTOM RELIEF
HEALING OF THE ULCER
PREVENTION OF RECURRENCE
PREVENT / THREAT COMPLICATION

H.PYLORI ERADICATION IS ESSENTIAL IN. H.PYLORY

POSITIVE PATIENTS
NSAID SHOULD BE DISCONTINUED OR REDUCED, IF POSSIBLE
PPIs ARE THE MOST EFFECTIVE AGENTS FOR ACID
SUPPRESSION AND THE MOST APPROPRIATE FIRST LINE
THERAPY.
Table : Management of peptic ulcer
Question: Action taken in the management
of ulcer
What type of ulcer?
- Gastric ulcer Requires biopsy to exclude
malignancy, requires
confirmation of healing by
endoscopy
- Duodenal Ulcer If symptoms resolve after
adequate treatment, endoscopy
generally not required except for
presentation with bleeding
Table : Management of peptic ulcer (Cont)
Question:
What the cause of ulcer disease?
- Has the patient used NSAID?
- Is H pylory infection present?
Any ulcerogenic risk factor?
- Aspirin or NSAID use
- Smoking
Action taken in the management of
ulcer
Evaluate for NSAID ingestion and H
pylori
If yes, evaluate indication for NSAID;
can this be stoped?
Treat H Pylori
Stop if possible; evaluate indication
and consider non-ulcerogenic
substitutes: eg, ticlopidine instead of
aspirin for cardiovascular prophylaxis;
non-NSAID analgesiscs such as
paracetamol or codein; COX-2
inhibitors
Advice to stop smoking
 THERAPY
- NON MEDICAMENT: Life style, Diiet

- MEDICAMENT:
. ANTACIDS
. CYTOPROTECTIVE AGENTS
Sucralfate, Misoprostol,Prostaglandin,Bismuth
subsalicylate,Treponene,Rebamipide.
. ACID SUPPRESSION
- ARH2 (Antagonis / Reseptor H2)
Cimetidin, Ranitidin, Famotidin.
- PPI (Proton Pump Inhibitors)
Omeprazole(20), Lansoprazole(30), Esomeprazole (20/40),
Rabeprazole(10), Pantoprazole(40).
Consensus of The Treatment H Pylori Infection
(Maastrich III-2005)
First Line Therapy For H Pylori Eradication
PPI- Clarithromycin Amoxicillin or metronidazole therapy remains the recommended
first line Therapy In populations with less than 15-20% clarithromycin resistance
prevalence in population in Less than 40% Metronidazole resistance prevalence
PPI clarithromycin - metronidazole is preferable

Quadriple therapies are alternative first line therapy

In case of failure

Second line therapy

Bismuth based quadruple therapies remain the best second line therapy, if available,
if not, PPI Amoxicillin or tetracycline and metronidazole are recommended

Subsequent failures rescue therapy

The rescue therapy should be based on antimicrobial susceptibility testing

Peter Malfertheiner, The 6th western Pasific Helicobacter Congress, 2006

 H Pylori Eradication (KSHPI)
Tripple therapy (1 or 2 weeks):
PPI + Amoxicillin + Clarithromycin
PPI + Metronidazole + Clarithromycin
PPI + Metronidazole + Tetracyclin (Alergy to clarithromycin)
Quadripple therapy ( 1 or 2 weeks):
If fail to therapy combination 3 drugs:
Bismuth + PPI + Amoxicillin + Clarithromycin
Bismuth + PPI + Metroniudazole + Clarithromycin
High resistency area:
PPI + Bismuth + Tetracyclin + Metronidazole
PPI 2 x/d: Omeprazole/Esomeprazole 20 mg, Lansoprazole 30 mg,
Pantoprazole 40 mg, Rabeprazole 10 mg
Amoxicillin 2 x 1000 mg/d, Clarithromycin 2 x 500 mg/d, metronidazole 3 x
500 mg/d, tetracyclin 4 x 250 mg/d, Bismuth 4 x 120 mg/d
Management of Uncomplicated Gastric Ulcer
**Gastric ulcer on endoscopy or barium meal

IS H PYLORI PRESENT?

Yes No

Eradication Treatment Is Patient taking NSAID?

If so, Stop NSAID

Successful *Unsuccessful

ANTI-SECRETORY TREATMENT 4-8 WEEKS

Repeat gastrocopy or barium

meal to asses healing

Healed Not Healed

Follow-Up Continue treatment

Consider repeat Bx To exclude cancer

Consider Surgery
Notes: *Quadriple therapy given for failed triple
**Gastric ulcer should be biopsied to exclude malignancy
Management of Uncomplicated Duodenal Ulcer
Duodenal Ulcer of Endoscopy or barium meal

Is H pylori Present

Yes No

Is patient taking NSAIDS?

Eradication Treatment
If so, stop NSAIDS

Successful & Unsuccessful* or

Symptoms resolve still symptomatic

optional Anti-secretory treatment 4-6 weeks

Low probability of recurence Review symptomps

No maintenance treatment And follow-up
 COMPLICATION

- HEMORRHAGE
CAUSED BY ULCER EROSING BLOOD VESSEL WALL;MAY RESULT IN DEATH

- PERFORATION
CAUSES SUDDEN INTENSE PAIN AS GUT CONTENTS ESCAPE INTO
ABDOMINAL CAVITY;REQUIRES HOSPITALISATION AND USUALLY
SURGERY
- OBSTRUCTION
SCARRING BLOCK STOMACH OUTLET, PREVENTING FOOD
PASSAGE, PATIENT EXPERIANCE VOMITING AND WEIGHT LOSS
CAVITY, REQUIRES HOSPITALISATION AND USUALLY SURGERY

- PENETRATION
ADJACENT VISCUS,LIVER,PANCREAS OR BILLIARY SYSTEM
 MANAGEMENT PUD WITH
COMPLICATION
SURGICAL ULCER
TOTAL GASTRECTOMY

ANTRECTOMY
VAGOTOMY
PYLOROPLASTY
CLOSE PERFORATION
BILLROTH I AND II
 REFRACTER ULCER
Helicobacter Pylori resistency of antibiotics
NSAIDs
Zollinger Ellison Syndrome/Gastrinoma
Gastric Cancer (Adenocarcinoma & Lymphoma)
Ischemic Gastropathy
Crohns Disease
Gastris Syphillis
Idiopathic Granulomatous Gastritis
Esinophilic Granulomatous Gastritis
Gastric Sarcoidosis
Gastric Tuberculosis
Viral infection: CMV & HSV
Amyloidosis
 REFRACTEC ULCER: 5 - 10% of ulcer
unhealed with conventional therapy.
Duodenal ulcer that not healed after 2 months
of H2RA therapy or 6 weeks of PPI or
Gastric ulcer that not healed after 3 months of
H2RA therapy or 8 weeks of PPI
The majority of ulcer patients become
asymptomatic within a few days of institution of
treatment.
About 95% of all ulcer will heal if therapy is
continued for up to 12 weeks.
 The Refractory Ulcer
> 12 weeks
compliance ?
optimal dose ?
Incorrect Diagnosis ( IBS / GC )
Eradication HP
Another cause : NSAID ?, cigarette ?, alcohol ?
Operation: perforation, Haemoragis, stenosis, refractory
 ZOLLINGER ELLISON SYNDROME
(GASTRINOMA)

Cause gastrin-secretin gut neuroendocrine

tumors (gastrinomas)
Ulcers solitary in distally duodenum, giant
ulcers >2 cm
Laboratory fasting serum gastrin >150 pg/mL
(500-700 pg/mL),Bacal acid output over 15
mEq/h.
 THERAPY
PPIs, 40 120 mg/day,complte
symptomrelief,ulcer healing
Patient with isolated hepatic metastase, surgical
resection.
Role of surgery, patient do not respond with
aggresive medical therapy.
Total gastrectomy,highly selective vagotomy.