CURRICULUMVITAE

Nama TempatLahir Agama AlamatRumah Alamatkantor PendidikanTerakhir Status

:Dr.SutantoMaduseno,SpPDKGEH :Yogyakarta :Islam :Jl.TegalsariNo.6RT09/RW30,Jl.PalaganTentaraPelajarYogyakarta :RSUPDr.Sardjito :Sp2KonsultanGastroenterohepatologi :Menikah

PENDIDIKAN SDJetis Harjo 1 Yogyakatta SMPNV Yogyakarta SMAIII Yogyakarta FKUGM Yogyakarta Spesialis Penyakit Dalam FKUGM Sp2KonsultanFKUI RIWAYATJABATAN Kepala Poliklinik Penyakit Dalam RSUPDr.Sardjito Yogyakarta,tahun 2002 2009 Wakil Kepala Instalasi Rawat Jalan RSUPDrSardjito Yogyakarta.Tahun 20032004. KepalaInstalasiRawatJalanRSUPDr.SardjitoYogyakarta,tahun2004 2009 KetuatimpengujikesehatanuntukwilayahPropinsiDaerahIstimewaYogyakartatahun20062009 DirekturMedikdanKeperawatanRSUPDrSardjito,tahun2009sekarang ORGANISASIPROFESI (CabangYogyakartadanNasional) AnggotaIkatanDokterIndonesia(IDI) PengurusPerhimpunanSpesialisPenyakitDalam(PAPDI)cabangYogyakarta SeksiPenelitianPengurusBesarPGIJakarta SeksiHumasPengurusBesarPPHIJakarta PengurusIkatanRematologiIndonesiacabangYogyakarta AnggotaPengurusCabangPPHIPGIPEGIYogyakarta ORGANISASISOSIALDANPENGHARGAAN AnggotadonordarahtetapPMIcabangKotaYogyakartasejaktahun1979,dansaatinitelahmenyumbangdarahsebanyak95 kali MendapatpenghargaansebagaidokterpuskesmasTeladanKabupatenMadiundanPropisiJawaTimurpadatahun1987

BySutantoMaduseno DivofGastrohepatology,DepartofInternal Medicines,FacultyofMedicine,GadjahMada University/SardjitoGeneralHospital Yogyakarta

DYSPEPSIA
DEFINITION:

Symptomslikepainornauseainepigastrium accompaniedbydisgust,vomit,bloat,easytofull, fullnessornitre,whichissuspectedcomefromthe abnormalityofuppergastrointestinaltractus(SCBA)

Dyspepsia: pathogenicmechanisms
Dysmotility H.pylori infection/ inflammation Mechanismsof dyspepsia Alteredgastric acidsecretion

Psychosocial factors

Guthypersensitivity
Witteman&Tytgat,NetherlandsJMed 1995;46:20511. Talleyetal.,BMJ 2001;323:12947. Tack etal.,CurrGastroenterolRep 2001;3:5038.

Dyspepsia: symptomassessment
Natureofsymptoms
Character Radiation Timing,duration andfrequency Modifyingfactors

Severityof symptoms

Assessment ofsymptoms

Patientsdegree ofdistress

Alarmfeatures

Par,CanJGastroenterol 1999;13:64754.

Ethiology
OrganicDyspepsia: Thereisanorganabnormalityasulcergastroduodenal, gastroesofageal refluxs andgastriccarcinoma(Talley, 1998)

WhatisFunctionalDyspepsia?
Persitentorrecurrentpainordiscomfortcenteredin

theupperabdomen
12weekswithinprevious12months Noevidenceoforganicdiesease Norelationbetweendyspepticsymptomsandbowel

movements(IBS). Exclusionofpatientswithdominantheartburn

symptomsofdyspepsiavs.diagnosisoffunctional

dyspepsia

FunctionalDyspepsia

Acommontermwhichisgiventothepatientas: abdominalpainornauseaontheupperofstomachwhich isrepeatedlyhappenmorethanthreemonths,andatleast alongofthattime25%symptomsofdyspepsiaappearand noevidenceorganicdiseasewhichisresponsibletothat symptomsclinically,biochemistrically,endoscopyand ultrasonografy(Talleyetal,1991).But,patientwith gastritisandduodenitisnonerosifisincludedinthisterm (Hu&Kren,1998)

DyspepsiaSubgroups
Dysmotilitylike Ulcerlike Unspecified

RomeIIIDiagnosticCriteriaforFunctional Dyspepsia
Functional Dyspepsia At least 3 months, with onset at least 6 months previously, of 1 or more of the following: Bothersome postprandial fullness Early satiation Epigastric pain Epigastric burning And No evidence of structural disease (including at upper endoscopy) that is likely to explain the symptoms

RomeIIIDiagnosticCriteriaforEpigastric PainSyndrome
Epigastric Pain Syndrome
At least 3 months, with onset at least 6 months previously, with ALL of the following: Pain and burning that is: intermittent localized to the epigastrium of at least moderate severity, at least once per week, and NOT: generalized or localized to other abdominal or chest regions 2. relieved by defecation or flatulence 3. fulfilling criteria for gallbladder or sphincter of Oddi disorders

RomeIIIDiagnosticCriteriafor PostprandialDistressSyndrome
Postprandial Distress Syndrome At least 3 months, with onset at least 6 months previously, of 1 or more of the following: Bothersome postprandial fullness 1. occurring after ordinary-sized meals 2. at least several times a week Early satiation 1. that prevents finishing a regular meal 2. and occurs at least several times a week

Clasification
acutedyspepsia(newonsetdyspepsia) SuddenlySighwiththequalityofsighwhichisusually moretremendouswithalongerresponsetothe medication. chronicdyspepsia Sighwhichissometimesdissappear,sometimesappear, morethantwoweeks.Thesighisnotastremendousas acutedyspepsiawithaquickresponsetothe medication.

Agresif Factor

Defensif Factor

AgresifFactor
GastricAcid Pepsin Refluxsbile Nicotin Alcohol Antiinflamationnonsteroid medicine Cortikosteroid Helicobacterpylori Freeradical

DefensifFactor Mucosabloodcurrent (microsirculation) Superficialepithelcell Prostaglandin Fosfolipid/Surfactans Musin Bikarbonat Motilitas

Diagramoftheequlibriumtheoryofintegrationgastrointestinal tractusmucosaespeciallygastric&duodenum

Parietal cell

H+ Proton pump Inhibitor

ClCl-

H+K+ATPase

(-)

K+

(-)
Gastrin Acetylcholine Histamine

Antagonist H2

Parietal Cell and proton pump (H+, K+-ATPase) (Robinson, 1999)

Gastritis; Should we follow symptoms or signs?

Symptom complex Endoscopic findings Microscopic inflammations

Clinicallyappearance ofChronicgastritis
Dyspesia Painpattern:painfoodpain notalways

happen,ifhappen patognomonis. Painfoodrelief duodeniulcers. TrueDiagnosis:endoscopy biopsy PA algoritmadyspesia

Presenceofsymptomsinpatientswith functionaldyspepsia

TackJ,etal.Gastroenterology2001;121:52635

Gastritis

Endoscopy(ExaminationIndication)
AnegativeresultoradoubtresultofRadiology Examination: toosmall&toosuperficial 2. IndicationoperationofGastriculcerorputaside thevicious 3. Lookagainifthemedicalmedicationisnot successed 4. DeterminethesourceofHemorrhage
1.

MechanismofAcidSecretion
Gastricphase
FoodinGaster ParietalCell

Cephalicphase
Nervus Vagus Asetilcholine

Gcell Gastrin ECLcell Histamine

MechanismofAcidSecretion
Gastricphase
FoodinGaster ParietalCell
HCl Cl

Cephalicphase
Nervus Vagus Asetilcholine

Gcell Gastrin
H+ H+ H+

K+

ECLcell Histamine

MechanismofAcidSecretion
Gastricphase
FoodinGaster ParietalCell

Cephalicphase
Nervus Vagus Asetilcholine

Gcell Gastrin ECLcell Histamine

MechanismofAcidSecretion
Gastricphase
FoodinGaster ParietalCell
HCl Cl

Cephalicphase
Nervus Vagus Asetilcholine

Gcell Gastrin
H+ H+ H+

K+

ECLcell Histamine

Algoritmofdyspepsiamanagement inthepublic
DYSPEPSIA
AGE < 45 YEARS WITHOUT NATURAL SIGNS AGE > 45 Years with Natural signs : - vomiting - fever - hematemesis - ictherus - Loose of body Weight The history of using chronic OAINS The hystory og gastric cancer in the family pasient is too worry with his disease

Empiric Therapy for 2 weeks with : - antacid - H2 antagonist/PPI - Prokinetic fail or exacerbation cured therapy is stopped exacerbation

serology Test of H.pylori

Referral centre : gastroenterologist / internist/ pediatrics with Endoscopy facility referral

result (-)

result (+)

exacerbation more than 3 times

1.GoalofPharmacotherapyindyspepsia
Controlsymptoms Promotehealing Preventcomplications Improvehealthrelatedqualityoflife AvoidAdverseeffectsoftreatment

DYSPEPSIA
Pharmacotherapy
Antacids AcidSuppressiondrug Prokineticagent Surfaceagent

Dyspepsia Treatment
1.

Antacida
Can be Tab/gel. The best is gel. Dossage : (15-30) cc 3-4 times a day, an hour after eat. (cheap, low complience)

2. The partition of H2-Receptor

Cimetidin dossage 2x (200-400) mg every morning and night or 800 mg at night b. Ranitidin dossage 2x (150-300) mg every morning and night or (300-600) mg at night c. Famotidin dossage 200 mg everyday
a.

3.

Motilitas Group

Donperidon 3x1 Cisapride 3x (5-10) mg/day

4. Prostaglandin E Group

Misoprostol emprostil

5. Sitoprotectif :

Sukralfat, setraksat, Teprenon 6. Others Medicine :

Anti anxiety Anti depresi Anti Convulsant

7. If needed :

Surgical therapy : vagotomi

MedicinetoControlGastricAcid
Antacida (cheap,lowcompilance,inefectiveforgastric ulcers,notconsistenceinmaintaningpH Intragastric,interactionwithothersdrugs,canbe usedinesofagitisrefluxslightly/moderate) AntagonistreseptorH2 (Cimetidine,ranitidine,famotidine) (consistenceinmaintainingpHIntragastric48 hours,lessefectiveatmealstimulatedanddaytime acidsecretion,easytotakhifilaksis,inefectiveto protectgastriculcersfortheOAINSusers,canbe usedinesofagitisrefluxslightly/moderate)

Table8.ThePossibilityoftheSideeffectthatcanappear afterusingmedicinewhichcontrolgastricacid
Drugs to control gastric acid Antagonist histamin2H receptor: Proton Pomp barrier : The possibility Side effect headache, dizziness, nausea, mialgia, skin rash, and itchy Nausea, diarrhea, can be abdominal cholic. headache, dizziness, and somnolen seldom to see the light rising of transaminase serum Sukralfat seldom give Side effect, if happen : constipated or dryness on mouth, sometimes abdominal discomfort. No serious side effect caused by teprenone except the rise of aminotransferase serum.

Sitoprotektif drugs :

(Shirakabe, 1995; Brunton, 1996)

Acidsupressiondrugs:
H2RA(H2 ReceptorAntagonist)
Cimetidine Ranitidine Famotidine Nizatidine

PPI(ProtonPumpInhibitor)
Omeprazole Lansoprazole Pantoprazole Rabeprazole Esomeprazole

TrendsinPrescribingofProtonPumpInhibitors inGeneralPracticeinEngland
Newer PPIs offer no advantage in terms of clinical efficacy over established PPIs, are usually more expensive and have less evidence for long-term safety.
MeReC Bulletin 2006;16:9-12

TotalExpenditureofOTCAntisecretory Therapy,USA,20032006

PPIbioavailabilityafterthefirstdose

90 80 Bioavailability(%) 70 60 50 40 30 20 10 0

80

77 64 52 40

Lansoprazole Pantoprazole Esomeprazole

Rabeprazole

Omeprazole

Tolman etal,JClin Gastroenterol 1997;24:6570. Fitton &Wiseman,Drugs 1996;51:46082. HassanAlin etal,Gastroenterology 2000;118:A16. Swanetal.,AlimentPharmacol Ther 1999;13(Suppl 3):117. Howden,Clin Pharmacokinet 1991;20:3849.

Matur Nuwun