dyspepsia dr maduseno sp pd
TRANSCRIPT
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CURRICULUMVITAE Nama : Dr.SutantoMaduseno,SpPDKGEH
TempatLahir :Yogyakarta
Agama :Islam
AlamatRumah
:Jl.Tegalsari
No.
6RT
09/RW
30,
Jl.
Palagan
Tentara
Pelajar
Yogyakarta
Alamatkantor :RSUPDr.Sardjito
PendidikanTerakhir :Sp2KonsultanGastroenterohepatologi
Status :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
ORGANISASISOSIAL
DAN
PENGHARGAAN
AnggotadonordarahtetapPMIcabangKotaYogyakartasejaktahun1979,dansaatinitelahmenyumbangdarahsebanyak95 kali
MendapatpenghargaansebagaidokterpuskesmasTeladanKabupatenMadiundanPropisiJawaTimurpadatahun1987
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By
Sutanto
MadusenoDivofGastrohepatology,DepartofInternalMedicines,FacultyofMedicine,GadjahMada
University/SardjitoGeneralHospital
Yogyakarta
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DYSPEPSIADEFINITION:
Symptomslikepainornauseainepigastrium
accompaniedby
disgust,
vomit,
bloat,
easy
to
full,
fullnessornitre,whichissuspectedcomefromtheabnormalityof uppergastrointestinaltractus(SCBA)
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Dysmotility
H.pyloriinfection/
inflammation
Psychosocialfactors
Alteredgastricacidsecretion
Guthypersensitivity
Mechanismsof
dyspepsia
Witteman&Tytgat,NetherlandsJMed1995;46:20511.Talleyetal.,BMJ2001;323:12947.
Tacketal.,CurrGastroenterolRep2001;3:5038.
Dyspepsia:pathogenicmechanisms
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Natureofsymptoms
Patientsdegreeofdistress
Severityofsymptoms
Alarmfeatures
Assessment
ofsymptoms
CharacterRadiationTiming,durationandfrequency
Modifyingfactors
Par,CanJGastroenterol1999;13:64754.
Dyspepsia:symptomassessment
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Ethiology
Organic
Dyspepsia
: Thereisanorganabnormalityasulcergastroduodenal,
gastroesofageal refluxs andgastriccarcinoma(Talley,
1998)
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WhatisFunctionalDyspepsia?Persitentorrecurrentpainordiscomfortcenteredin
theupperabdomen 12weekswithinprevious12months
Noevidenceoforganicdiesease
Norelationbetweendyspepticsymptomsandbowelmovements(IBS).
Exclusionofpatientswithdominantheartburn
symptomsofdyspepsiavs.diagnosisoffunctionaldyspepsia
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FunctionalDyspepsia Acommontermwhichisgiventothepatientas:
abdominalpainornauseaontheupperofstomachwhich
isrepeatedlyhappenmorethanthreemonths,andatleast
alongofthattime25%symptomsofdyspepsiaappearand
noevidenceorganicdiseasewhichisresponsibletothat
symptomsclinically,biochemistrically,endoscopyand
ultrasonografy(Talleyetal,1991).But,patientwithgastritisandduodenitisnonerosifisincludedinthisterm
(Hu&Kren,1998)
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DyspepsiaSubgroupsDysmotilitylike
Ulcerlike
Unspecified
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RomeIII
Diagnostic
Criteria
for
Functional
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 burningAnd
No evidence of structural disease (including at upper
endoscopy) that is likely to explain the symptoms
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RomeIII
Diagnostic
Criteria
for
Epigastric
PainSyndromeEpigastric 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
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RomeIII
Diagnostic
Criteria
for
PostprandialDistressSyndromePostprandial Distress SyndromeAt 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
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Clasificationacutedyspepsia (newonsetdyspepsia)
SuddenlySighwiththequalityofsighwhichisusuallymoretremendouswithalongerresponsetothemedication.
chronicdyspepsia Sighwhichissometimesdissappear,sometimesappear,
more
than
two
weeks.
The
sigh
is
not
as
tremendous
as
acutedyspepsiawithaquickresponsetothemedication.
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AgresifFactor GastricAcid Pepsin Refluxsbile
Nicotin Alcohol Antiinflamationnonsteroid
medicine Cortikosteroid
Helicobacterpylori Freeradical
Agresif Factor Defensif Factor
DefensifFactorMucosabloodcurrent(microsirculation)
Superficial
epithel
cellProstaglandinFosfolipid/SurfactansMusinBikarbonat
Motilitas
Diagramoftheequlibriumtheoryofintegrationgastrointestinal
tractus
mucosa
especially
gastric
&
duodenum
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Proton pump
Inhibitor
Gastrin Acetylcholine Histamine
AntagonistH2
H+K+ATPase
H+ Cl-
Cl-
(-)
(-)K+
Parietal cell
Parietal Cell and proton pump (H+, K+-ATPase)
(Robinson, 1999)
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Gastritis; Should we follow symptoms orsigns?
Symptom complex
Endoscopic findings
Microscopic inflammations
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Clinicallyappearance
ofChronicgastritisDyspesia
Painpattern
:pain
food
pain
not
always
happen,ifhappen patognomonis.
Painfoodrelief duodeniulcers.
TrueDiagnosis:endoscopy biopsy PAalgoritmadyspesia
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Presenceof
symptoms
in
patients
with
functionaldyspepsia
TackJ,etal. Gastroenterology2001;121:52635
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Gastritis
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Endoscopy(ExaminationIndication)1. AnegativeresultoradoubtresultofRadiology
Examination:
toosmall&toosuperficial
2. Indication
operation
of
Gastric
ulcer
or
put
aside
thevicious
3. Lookagainifthemedicalmedicationisnot
successed
4. DeterminethesourceofHemorrhage
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MechanismofAcidSecretion
CephalicphaseGastricphaseNervus Vagus
Asetilcholine
ECLcell
Histamine
FoodinGaster
Gcell
Gastrin
ParietalCell
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Nervus Vagus
ECLcell
Gcell
Gastrin H+
K+
Cl
H+
H+
HCl
MechanismofAcidSecretion
CephalicphaseGastricphase
Asetilcholine
Histamine
FoodinGaster ParietalCell
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MechanismofAcidSecretion
CephalicphaseGastricphaseNervus Vagus
Asetilcholine
ECLcell
Histamine
FoodinGaster
Gcell
Gastrin
ParietalCell
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Nervus Vagus
ECLcell
Gcell
Gastrin H+
K+
Cl
H+
H+
HCl
MechanismofAcidSecretion
CephalicphaseGastricphase
Asetilcholine
Histamine
FoodinGaster ParietalCell
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Algoritmofdyspepsiamanagementinthepublic
DYSPEPSIA
AGE < 45 YEARSWITHOUT 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 cured
- H2 antagonist/PPI
- Prokinetic therapy is stopped
fail or exacerbation exacerbation
serology Test of H.pyloriReferral centre : gastroenterologist
/ internist/ pediatrics with
Endoscopy facility
result (-) result (+) referral
exacerbation more than 3 times
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1.GoalofPharmacotherapyindyspepsia
Controlsymptoms
Promote
healing Preventcomplications
Improvehealthrelatedqualityoflife
AvoidAdverseeffectsoftreatment
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Pharmacotherapy
Antacids
Acid
Suppression
drugProkineticagent
Surfaceagent
DYSPEPSIA
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Dyspepsia Treatment1. 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)
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2. The partition of H2-Receptora. Cimetidin
dossage 2x (200-400) mg every morning and night
or 800 mg at nightb. Ranitidin
dossage 2x (150-300) mg every morning and night
or (300-600) mg at nightc. Famotidin
dossage 200 mg everyday
3. Motilitas Group Donperidon 3x1
Cisapride 3x (5-10) mg/day
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4. Prostaglandin E Group Misoprostol
emprostil
5. Sitoprotectif :
Sukralfat, setraksat, Teprenon
6. Others Medicine : Anti anxiety
Anti depresi
Anti Convulsant7. If needed :
Surgical therapy : vagotomi
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MedicinetoControlGastricAcidAntacida
(cheap,low
compilance,
inefective
for
gastric
ulcers,notconsistenceinmaintaningpHIntragastric,interactionwithothersdrugs,canbeusedinesofagitisrefluxslightly/moderate)
AntagonistreseptorH2(Cimetidine,ranitidine,famotidine)
(consistenceinmaintainingpHIntragastric48
hours,less
efective
at
meal
stimulated
and
day
time
acidsecretion,easytotakhifilaksis,inefectivetoprotectgastriculcersfortheOAINSusers,canbeusedinesofagitisrefluxslightly/moderate)
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Table8.ThePossibilityof theSideeffectthatcanappearafterusingmedicinewhichcontrolgastricacid
Drugs to control
gastric acidThe possibili ty Side effect
Antagonist histamin2Hreceptor:
Proton Pomp barrier :
Sitoprotektif drugs :
headache, dizziness, nausea, mialgia, skinrash, and itchy
Nausea, diarrhea, can be abdominal cholic.
headache, dizziness, and somnolen seldom tosee the light rising of transaminase serum
Sukralfat seldom give Side effect, if happen :
constipated or dryness on mouth, sometimes
abdominal discomfort. No serious side effectcaused by teprenone except the rise of
aminotransferase serum.
(Shirakabe, 1995; Brunton, 1996)
d d
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Acidsupressiondrugs:
H2RA(H2ReceptorAntagonist)
PPI(ProtonPumpInhibitor)
Cimetidine
RanitidineFamotidine
Nizatidine
Omeprazole
LansoprazolePantoprazole
Rabeprazole
Esomeprazole
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TrendsinPrescribingofProtonPumpInhibitorsinGeneralPracticeinEngland
Newer PPIs offer no advantage in terms of
clinical efficacy over established PPIs, are
usually more expensive and have lessevidence for long-term safety.
MeReC Bulletin 2006;16:9-12
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TotalExpenditureofOTCAntisecretoryTherapy,USA,20032006
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Bioavailability(%)
Tolmanetal,JClin Gastroenterol1997;24:6570.Fitton &
Wiseman,
Drugs1996;
51:
46082.HassanAlinetal,Gastroenterology 2000;118:A16.
Swanetal.,AlimentPharmacol Ther1999;13(Suppl 3):117.Howden,Clin Pharmacokinet1991;20:3849.
PPIbioavailabilityafterthefirstdose
8090
80
70
60
50
4030
20
10
0
Lansoprazole Pantoprazole Esomeprazole Rabeprazole Omeprazole
77
64
52
40
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Matur
Nuwun