DEFINISI

KUMPULAN GEJALA, BERSIFAT EPISODIK/

MENETAP YG SELALU MENYERTAKAN
NYERI/TIDAK NYAMAN DI PERUT BAGIAN
ATAS.
NYERI ULU HATI,MUAL,KEMBUNG,RASA
PENUH,SENDAWA.

KRITERIA-ROMA II 2000,DYSPEPSIA REFERS

TO PAIN OR DISCOMFORT CENTERED IN THE
UPPER ABDOMEN. HEART BURN OR PIROSIS
IS EXCLUDE.
Definition of dyspepsia (Rome II)

Pain or discomfort occurring

in the upper abdomen

Dyspepsia subgroups
 Ulcer-like (predominantly pain)
 Dysmotility-like (predominantly discomfort)
 Unspecified (non-specific, no predominant
symptom)

Talley et al., Gut 1999; 45(Suppl II): II37–42.

Malfertheiner, Eur J Gastroenterol Hepatol 1999; 11(Suppl 1): S25–9.
 CRITERIA “ ROME III “

• INTERNATIONAL CONSENSUS REPORT CALLED “

rome III “.focusing on two grups of symptoms :

1.Meal-induced symptoms such as : post prandial

fullness and early satiation.

2.Epigastric pain and epigastric burning.

 PENYEBAB

DISPEPSIA ORGANIK

DISPEPSIA FUNGSIONAL
 DISPEPSIA ORGANIK

Apabila pada pemeriksa’an yang lebih lengkap

ditemukan kelainan organ

Gastritis
Duodenitis
TUKAK LAMBUNG/DUODENUM
Tumor
Bile refluk
Helikobakter Pylori
DISPEPSIA FUNGSIONAL

YAITU DISPEPSIA YANG SUDAH DIPERIKSA

SECARA LENGKAP ,TIDAK DITEMUKAN ADA
NYA KELAINAN ORGANIK.
DISPEPSIA SECARA UMUM ,DIBAGI :

DISPEPSIA –LIKE ULCER

DISPEPSIA – LIKE DISMOTILITY
DISPEPSIA NON SPESIFIK
DIAGNOSIS & PENDKTN KLINIK

ANAMNESE:
MENDUKUNG/MEMBERI
PETUNJUK UNTUK
MEMBANTU
DIAGNOSIS:

TUKAK LAMBUNG :
GEJALANYA NYERI
ULUHATI PADA MALAM
HARI,NYERI HILANG
WAKTU MAKAN,NYERI
YG MENUSUK DSB.
 PATO FISIOLOGI

BELUM DIMENGERTI SECARA PENUH

DIDUGA: PENGOSONGAN LAMBUNG YANG
LAMBAT,PENINGKATAN TEKANAN DALAM
LAMBUNG&PENINGKATAN TONUS OTOT
PERUT RASA PENUH/KEMBUNG.
MELIPUTI:DISFUNGSI OTOT POLOS,PENGOSONGAN
LAMBUNG,PERMEABILITAS MUKOSA ABNORMAL
ASAM LAMBUNG MASUK KEDINDING LAMBUNG
KERUSAKAN SISTEM SARAF, RE MODELLING
SARAF dsb.
H. PYLORI
PSIKOGENIK
DLL
 Dyspepsia:
pathogenic mechanisms

Dysmotility
H. pylori infection/ Altered gastric
inflammation acid secretion

Mechanisms of
dyspepsia

Psychosocial Gut hypersensitivity

factors
Witteman & Tytgat, Netherlands J Med 1995; 46: 205–11.
Talley et al., BMJ 2001; 323:1294–7.
Tack et al., Curr Gastroenterol Rep 2001; 3: 503–8.
 PENDEKATAN KLINIK

KEGANASAN: ADA TANDA ALARM,MUNTAH

WARNA HITAM,B.AB. WARNA HITAM

RIWAYAT MINUM OBAT2AN: GASTRITIS

EROSIF

MENCARI PENYEBAB : ENDOSKOPI DAN

RADIOLOGI
Dyspepsia covers a range of symptoms

DYSPEPSIA
GORD PAIN OR DISCOMFORT IBS
centred in upper abdomen

UNINVESTIGATED INVESTIGATED

ORGANIC FUNCTIONAL
(or idiopathic)
(use of the term ‘non-ulcer’
is discouraged)

Talley et al., Gut 1999; 45(Suppl II): II37–42.

Differential diagnosis of dyspepsia

Functional dyspepsia
GORD
PUD
Gastric malignancy
Pancreatitis
Musculoskeletal pain
IBS
Cardiovascular disease
Somatisation
Pancreato-biliary disease

Talley et al., BMJ 2001; 323: 1294–7.

 SKEMA PENATALAKSANAAN PASIEN DI PELAYANAN
KESEHATAN LINI PERTAMA

DISPEPSIA

UMUR < 45 TH TANPA TANDA BAHAYA UMUR > 45 ATAU < 45 DGN TANDA BAHAYA

TERAPI EMPIRIS SLM 2 MGG:

 ANTASID DISPEPSIA (-) TERAPI DIHENTIKAN
 H2 ANTAGONIS
 PPI DISPEPSIA (+)
 OBAT2 PROKINETIK

SEROLOGI (TERVALIDASI SECARA LOKAL)

ENDOSKOPI HASIL (+) HASIL (-)

TIDAK ADA SARANA RUJUK:

INTERNIS, INTERNIS PLUS, GASTROENTEROLOGIST
UBT / HpSA ATAU DOKTER ANAK DENGAN FASILITAS ENDOSKOPI

HASIL (-) HASIL (+) TERAPI ERADIKASI

GAGAL
 SKEMA PENATALAKSANAAN PASIEN DISPEPSIA OLEH
GASTROENTEROLOGIS/INTERNIS DENGAN FASILITAS ENDOSKOPI

DISPEPSIA

UMUR > 45 TH
“TANDA BAHAYA”
GAGAL TERAPI
TIDAK RIWAYAT ULKS PEPTIKUM + KOMPLIKASI YA
PERMINTAAN PASIEN
PENGGUNA ASPIRIN/NSAID
GASTROESOPHAGEAL REFLUX DISEASE (GERD)
UBT / HpSA ENDOSKOPI

HASIL HASIL PEMERIKSAAN RAPID UREASE TEST

(-) (+) (CLO, MU, PROTONDRY*)
HISTOPATOLOGY

HASIL (+) HASIL (-)

TERAPI ERADIKASI TERAPI SIMTOMATIK

REEVALUASI DIAGNOSTIK

TERAPI SIMTOMATIK GAGAL

 When to refer

Presence of alarm symptoms

Failure to respond to
appropriate therapy
Patients 45 years of age with
new-onset symptoms

Talley et al., Gut 1999; 45(Suppl II): II37–42.

Talley et al., BMJ 2001; 323: 1294–7.
Bytzer & Talley, Ann Intern Med 2001; 134: 815–22.
 TUKAK PEPTIK

TUKAK LAMBUNG

TUKAK DUODENUM
PATOFISIOLOGI DAN PATOGENESIS

KERUSAKAN PD PRINSIPNYA O.K. GGUAN

KESEIMBANGAN ANTARA FAKTOR DEFENSIF DAN
FAKTOR AGRESIF,UMUMNYA SBG AKIBAT
MELEMAHNYA FAKTOR DEFENSIF
TEORI LAMA’ NO ACID NO ULCER, DR SCWARTZ
(1910) TDK BENAR.
FISIOLOGI: MUKOSA LAMBUNG RESISTEN TERHADAP
PROSES OTODIGESTI DAN PUNYA MEKANISME
PERLINDUNGAN THDP PENGA RUH DR LUAR. APA
BILA FAKTOR KESEIMBANGAN TERGANGGU MAKA
DAYA TAHAN MUKOSA MENURUN TERJADILAH
GASTRITIS ATAU TUKAK PEPTIK
 FAKTOR DEFENSIF

1 RINTANGAN MUKUS ( MUCUS BARRIER)

2 BIKARBONAT: DIHASIL-SEL EPIT- LAMB-& DUOD-

3 PROSTAGLANDIN: DIHASILKAN SEL EPITEL LAMB-

4 ALIRAN DARAH MUKOSA

5 REGENERASI SEL: EPIT- MUKOSA GANTI 2-6 HARI

6 FAKTOR PERTUMBUHAN (GROWTH FAKT-)

 FAKTOR AGRESIF

1. FAKTOR KERUSAKAN MUKUS

2. PRODUKSI BIK-NAT YG MENURUN

3. ALIRAN DARAH MUKOSA YG TERGGGU

 FAKTOR AGRESIF

4. FAKTOR DARI LUAR( ASPIRIN,NSAID,

ROKOK,MINUMAN,STRESS DLL )

5 FAKTOR GENETIK.RIWAYAT KELUARGA

MEMPUNYAI RESIKO 3 X UTK TUKAK PEPTIK
DUODENUM LEBIH BESAR

6 HELIKOBAKTER PYLORI,DITEMUKAN
WARREN & MARSHAL 1983 DI AUSTRALIA
PRINSIP DASAR PENGOBATAN

1 MERINGANKAN/MENGHILANGKAN
KELUHAN ( RASA SAKIT )

2 KESEMBUHAN TUKAK

3 MENCEGAH TERJADINYA KOMPLIKASI

4 MENCEGAH TERJADINYA KEKAMBUHAN

OBAT OBAT YG TERSEDIA

ANTASIDA

H2 RESEPTOR ANTAGONIS

SUCRALFAT

PROSTAGLANDIN ANALOG

KOLOID BISMUTH

PROTON PUMP INHIBITOR ( PPI)

 Primary regions of gastric
acid-related disease

Acid reflux
Oesophagitis
Strictures
Barrett’s
oesophagus
Oesophageal Gastritis
adenocarcinoma
Peptic ulcer
disease
(Includes NSAID-
induced ulcers)
Functional
dyspepsia
Duodenitis
Duodenal ulcer
Management of
uninvestigated
dyspepsia
 GP management of
uninvestigated dyspepsia

Alarm features (and/or >45 years?) No alarm features (and/or <45 years?)

Refer/investigate Symptom-based diagnosis

4 weeks’ therapy based on predominant symptom

Treat accordingly
Responders Non-responders/early relapses

1st-line investigation (13CUBT/stool test)

H. pylori +ve H. pylori -ve

Eradication therapy

Responders Non-responders
2nd-line investigation Increase doses/combination therapies
Stanghellini, 2001.
Functional dyspepsia:
an exclusion diagnosis
 Causes of functional dyspepsia

Illness behaviour Symptom perception

Psychosocial factors

Genetic predisposition Spinal hyperalgesia

Intraluminal Altered motility

Noxious stimuli
(Food allergy? Visceral hypersensitivity
H. pylori?)
Gut wall inflammation
Treatment options in functional dyspepsia

Muco-protective Acid inhibition

agents

Functional
Functional
Dyspepsia
dyspepsia

Prokinetic motility H. pylori eradication

agents
Phytotherapeutics
Carminatives
Anti-depressants
Anti-serotoninergics
Opioids
Talley et al., Aliment Pharmacol Ther 1999; 13: 1135–48.
Talley et al., Gut 1999; 45(Suppl II): II37–42.
Should we eradicate
H. pylori in functional
dyspepsia?
 H. pylori eradication in functional
dyspepsia: background

Large ‘optimised’ clinical trials give inconsistent

results for the long-term benefit of H. pylori
eradication on dyspeptic symptoms
3 ‘No’ 1 ‘Yes’
Blum et al., 1998 McColl et al., 1998
Talley et al., 1999
vs (single-centre trial)
Talley et al., 1999
(all multicentre trials)

If there is a benefit, it is limited to a

subgroup of patients
Blum et al., N Engl J Med 1998; 339: 1875–81.
Talley et al., BMJ 1999; 318: 833–7.
Talley et al., N Engl J Med 1999; 341: 1106–11.
McColl et al., N Engl J Med 1998; 339: 1869–74.
 ELAN study

Eradication versus
Lansoprazole in H. pylori-
Associated
Non-ulcer dyspepsia

Malfertheiner et al., Gastroenterology 2000; 118(Suppl 3): A440.

 Functional dyspepsia:
therapeutic strategy proposals

Endoscopy + biopsies

H. pylori-positive H. pylori-negative

Eradication PPI

No symptoms Symptoms Symptoms No symptoms

2nd/3rd-line options or
Other empirical therapy
Malfertheiner, 2001.
NSAIDs inhibit the COX enzyme, which
exists in two forms
Arachidonic acid

COX-1 COX-2
(constitutive) (induced by inflammatory stimuli)

COX-2 selective NSAIDs 

 Non-selective NSAIDs 
Prostaglandins Prostaglandins

• Gastrointestinal cytoprotection • Inflammation

• Platelet activity • Pain
• Fever
Adapted from Vane & Botting 1995
 Systemic effects of NSAIDs
may lead to gastric mucosal damage
NSAIDs

Altered inflammatory
mediator production
(e.g. decreased
prostaglandin, increased
tumour necrosis factor)

Increased neutrophil–
endothelial adhesion

Capillary obstruction Neutrophil release of

proteases and oxygen-
derived free radicals

Ischaemic/hypoxic cell Endothelial and epithelial

injury injury

Mucosal ulceration
Wallace 1997
Management of NSAID-induced
peptic ulcer disease

Discontinue use of NSAIDs or

substitute with less toxic agents
 Low-toxicity NSAIDs or COX-2 inhibitors

Suppress acid secretion

 Normal-dose PPI therapy
 High-dose H2RA therapy

Use mucosal protectants

 Misoprostol (substantial side-effects,
abortifacient)
Seager & Hawkey, BMJ 2001; 323: 1236–9.
Silverstein et al., Ann Intern Med 1995; 123: 241–9.
Graham et al., Ann Intern Med 1993; 119: 257–62.
Yeomans et al., N Engl J Med 1998; 338: 719–26.