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Erwin Budi Cahyono
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DEFINITION :
Symptoms like pain or nausea in epigastrium
accompanied by disgust, vomit, bloat, easy tofull, fullness or nitre, which is suspected comefrom the abnormality of upper gastro-intestinal tractus.
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Dysmotility
H. pylo r iinfection/
inflammation
Psychosocial
factors
Altered gastric
acid secretion
Gut hypersensitivity
Mechanisms of
dyspepsia
Witteman & Tytgat, Netherlands J Med1995; 46: 20511.
Talley et al., BMJ2001; 323:12947.Tack et al., Curr Gastroenterol Rep 2001; 3: 5038.
Dyspepsia:
pathogenic mechanisms
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Nature of symptoms
Patients degree
of distress
Severity of
symptoms
Alarm features
Assessment
of symptoms
Character
Radiation
Timing, duration
and frequency
Modifying factors
Par, Can J Gastroenterol1999; 13: 64754.
Dyspepsia:
symptom assessment
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acute dyspepsia (new onset dyspepsia) Suddenly sigh with the quality of sigh which is
usually more tremendous with a longer response tothe medication.
chronic dyspepsia Sigh which is sometimes disappear, sometimes
appear, more than two weeks. The sigh is not astremendous as acute dyspepsia with a quick
response to the medication.
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Organic Dyspepsia :
There is an organ abnormality as ulcer gastro-
duodenal, gastro esofageal reflux and gastriccarcinoma (Talley, 1998)
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A common term which is given to the patient as :
abdominal pain or nausea on the upper of stomach
which is repeatedly happen more than three months,
and at least a long of that time 25% symptoms ofdyspepsia appear and no evidence organic disease
which is responsible to that symptoms clinically,
biochemistrically, endoscopy and ultrasonografy
(Talley et al, 1991). But, patient with gastritis and
duodenitis non erosif is included in this term (Hu &
Kren, 1998)
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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
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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 regions2. relieved by defecation or flatulence
3. fulfilling criteria for gallbladder or sphincter of Oddi disorders
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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
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GASTRITIS
- Peradangan mukosa lambung (Dx PA)- Gastroskopi: eritema, edema, erosiva
- Klinik: keluhan dispepsia
Sering dijumpai dalam klinik:- Gastritis antrum, Gastritis erosiva,
- Gastritis hemoragika, Gastritis atropik, Penyebab:
- infeksi Helicobacter pylori, OAINS,- refluks empedu, obat lain, stress, alkohol
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ULKUS PEPTIK
Ulkus Peptik- Kerusakan (luka) mukosa, besar (> 5mm)
dan dalam (> submukosa), sifat jinak- Gastroskopi: bentuk ulkus- Klinik: keluhan dispepsia
Pembagian berdasarkan lokasi kelainan:- Ulkus Esofagus- Ulkus Gaster- Ulkus Duodenum
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* Sindroma Dispepsia
* Komplikasi : muntah, muntah/berak darah, nyeri hebat.
1. Keluhan / gejala
2. Tanda fisik
* Tidak jelas, nyeri tekan uluhati (hebatkomplikasi)
3. Radiologi (foto seri SCBA)
* Kontras tunggal akurasi rendah, sebaiknya kontr as ganda
* Gastr i tis (edema, hipersekresi), Ulkus (niche/ kawah ulkus)4. Gastroskopi
* Diagnosis utama, akurasi >95%,
* Dx. endoskopi, biopsi (PA, CLO, dll .)
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Multiple causes of gastritis/ peptic ulcer disease
Defensive
Aggressive
Gastric lumen
Mechanical stressChemicalIrritant (Alcohol, NSAIDs)Pepsin, Acid
H+
Pepsin, Acid
Solubilized mucus
H+
back
diffusion
Surface mucus
cell
Parietal
cell
Gland-type mucuscellChief cellShay & Suns
balance theory
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Agressive Factors Gastric Acid
Pepsin Refluxs bile
Nicotin
Alcohol
Antiinflamation nonsteroidmedicine
Cortikosteroid
Helicobacter pylo r i Free radical
Agresif Factor Defensif Factor
Defensive Factors
Mucosa blood current
(microsirculation)Superficial epithel cell
Prostaglandin
Fosfolipid/Surfactans
Musin
Bikarbonat
Motilitas
Diagram of the equlibrium theory of integration gastro-intestinal
tractus mucosa especially gastric & duodenum
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Surface epithelialcells
Mucus layer
Ionic gradientBicarbonate layer
Prostaglandins
Mucosal bloodsupply
NSAIDs
H . pyloriPepsinGastric
acid
Acidicenvironment
Neutral environment
Bile
AGGRESSIVE FACTORS
PROTECTIVE FACTORS
Imbalanced between aggressive factors and protective factors
Noxious agents
Pre-epithelial
Epithelial
Sub-epithelial
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H.Pylori cover, T.L., et al. :ASM Nwes, 61(!),21,1995
H.Pyloriinfection
MALT
Lymphoma
Chronic
SuperficialGastritis
Peptic
Ulcer Disease
Chronic Superficial Gastritis
(Histological Gastritis)
Gastric Cancer
Chronic
Atrophic
Gastritis
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Proposed natural history ofHelicobacter
pyloriinfection in humans
Childhood Old Age
Chronic Active GastritisAcuteGastritis
Environmental
Factors
MultifocalAtrophic
Gastritis
AntralPredominantGastritis
Gastric Cancer
Lymphoma
Gastric Ulcer
Duodenal Ulcer
Duodenitis
H.pylor i
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Test Sensitivity/specifity, % Comments
INVASIVE (ENDOSCOPY/BIOPSY REQUIRED)
Rapid urease
Histology
Culture
80 - 95/95 100
80 90/>95
--/--
Simple, false negative with recent use of PPIs,
antibiotics, or bismuth compounds
Requires pathology processing and informationTime-consuming, expensive, dependent on
experience; allows determination of antibiotic
susceptibility
NON-INVASIVE
Serology
Urea breath test
Stool antigen
>80/>90
>90/>90
>90/>90
Inexpensive, convenient; not useful for early
follow-up
Simple, rapid; useful for early follow-up; false
negatives with recent therapy (see rapid urease
test); exposure to low-dose radiation with 14C test
Inexpensive, convenient; not established for
eradication but promising
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Normal
mucosa
Superficial
gastritis
Atrophic
gastritis
Intestinal
metaplasiaDysplasia Gastric
adenoCa.
Salt Higher pH
Salt
N-nitroso carcinogensInflammatory cell carcinogens
Ascorbic acid -carotene H. pylo r i
Chronic atrophic gastritis Gastric ulcer Gastric adenoma with dysplasia Gastric cancer
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1. Menghilangkan keluhan
2. Mempercepat penyembuhan luka
3. Mengobati komplikasi
4. Mencegah kekambuhan
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Penting mencari:
- faktor-2 yang berperan pada penyakit
- diagnosis dan pengobatan yang sesuai
2. Merubah cara hidup (life style)
Faktor yang perlu diperbaiki a.l.:
- rokok, alkohol, diet, cara makan, dll.
- stress psiko-sosial
1. Pendekatan pribadi
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1. Antasida
2. Penghambat sekresi asama. Anti-muskarinik
b. Antagonis H2 -reseptor (H2RA)
c. Penghambat pompa proton (PPI)
Omeprazole, Rabeprazole, Pantoprazole, Lansoprazole(Prosogan FD R)
3. Sitoproteksi
a. Sucralfate
b. Cetraxatec. Colloidal Bismuth subcitrate
d. Prostaglandin
e. Teprenone
f. Rebamipide
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1. Antasida- netrali sir asam lambung, menghi langkan rasa sakit
2. Anti-kholinergik (muskarinik)
- pirenzepin: selekti f , ES ringan
3. Antagonis reseptor H2 (H2RA)
- Cime-, Rani-, Famo-, Roxa-, Niza-tidin
- efektif untuk pengobatan UP
- (80% UD 8 mgg, UG 12 mgg)
4. Penghambat pompa proton (PPI)
- Ome-, Lanso-, Panto-, Rabe-, Esome-prazol
- paling efekti f : UP, eradikasi H p, GERD
- > 90% UP sembuh, UD 4 mgg, UG 6 mgg
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Chronic inflammation is a major factor for thepathogenesis of serious gastroduodenaldiseases and in the long term, is one of themost important factor in carcinogenesis.
Alarm features require immediate referral to a
specialist for further investigation.
Helicobacter Pylori infection has a clinically
important mechanism of chronic inflamation. Proton pump inhibitors improve ulcers
healing and eradicate H. pylori moreeffectively.
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TERIMA KASIH
ATAS PERHATIANNYA
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Prevalensi ( Asia)
Heartburn,
Regurgitation
GERD Productivity
Quality of Life
Complication Troublesome Complication
Reflux of Stomach Contains
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Incompetence GEJ
Trans relax of LES Hiatus herniaHipotension of LES Short LES
Anatomic Disturbance drugs
Hormonal
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With Chest pain OesophagealOesophagitis (visceral errosions
hyperalgesia) & or ulcerswithout Hoarsrness stricturesOesophagitis (reflux
laryngitis) BarrettsAsthma, Oesophagus
Chronic cough,wheezing Oesophageal
dental adenocarcinomaNatheo, Int J Clin Pract errosions2001 ; 55 :465-9
Typical Symptoms(Heartburn/
Regurgitation)Atypical Symptoms Complications
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The Global Definition of GERD :GERD is a condition which develops when the reflux ofstomach contents causes troublesome symptoms and/ orcomplicationsSymptoms related to gastro-esophageal reflux becometroublesome when they adversly affect an individualswell-beingReflux symptoms that are not troublesome should not bediagnosed as GERDIn Clinical Practice, the patients should determine if theirreflux symptoms are troublesome
Schoeider HR. GERD. The Montreal definition and classification. SA Fam Pract 2007;49(1):19-26
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GERD is a condition which develops when the reflux
of stomach content causes trouble some symptomsand/or complications
Symptomatic
Syndromes
Extra-Esophageal
SyndromesEsophageal
Syndromes
Proposed
AssociationEstablished
Association
Syndromes with
Esophageal
injury
Typical RefluxSyndromes
Reflux Chest
Pain Syndromes
Refluks EsophagitisReflux Stricture
Barretts Esophageus
Adenocarcinoma
Reflux CoughReflux Laryngitis
Reflux asthma
Reflux dental Erotion
PharingitisSinusitis
Idiopathic
Pulmonary Fibrosis
Recurrent Otitis
Media
Vakil N et al. Am J Gastroenterol 2006;101:1900-1920
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GERD is a condition which develops when the
reflux of stomach contents causes troublesomesymptoms and/or complication
Vakil N et al. Am J Gastroenterol 2006;101:1900-1920
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Symptoms related to Gastroesophageal Refluxbecome troublesome when they adverselyaffect an individual well-being
.mild symptoms occuring 2 or more days aweek, or moderate/severe symptoms occuringmore than 1 day aweek, are often considered
troublesome by patient
Vakil N et al. Am J Gastroenterol 2006;101:1900-1920
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In clinical practice, the patient shoulddetermine if their reflux symptoms aretroublesome
Vakil N et al. Am J Gastroenterol 2006;101:1900-1920
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The Typical Reflux Syndrome can bediagnosed on the basis of characteristis
symptoms, without diagnostic testing
Heartburn and regurgitation are thecharacteristic symptoms of the Typical RefluxSyndrome
Vakil N et al. Am J Gastroenterol 2006;101:1900-1920
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*when cardiac causes have been excluded
Troublesome Symptoms
Heartburn Dysphagia-may indicate GERD
Epigastric pain
Regurgitation
Retrosternal pain*
(Chest Pain)
Extra-esophageal
symptoms(Chronic cough,
Hoarseness, etc)
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Dent J et al. Gut 2005 :54 :710-7
Mild or Infrequent
Significant impactsSevere or frequent
Minor Impacts
Mild or infrequent symptoms may, however,
indicate reflux disease if they have
a significant impact on a patients daily life
Not disease
Symptoms caused by gastroesopageal reflux
Reflux disease
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DeVault KR,Catell DO. Am J Gastroenterol 2005;100:190-200
Rao G.J Fam Pract 2005;54(12 suppl):3-8
Symptoms based
diagnosis
Reflux
Esophagitis
Non ErosiveReflux Disease
Treatment Failure
Endoscopy
Empirical Therapy
Complicated
Reflux Disease
Risk Assesment
Alarm Symptoms
~95% ofPatients in
Primary
care
~5%
~35%
~60%
Adapted from Lebenz J et al.World JGastroenterol.2005;11:
4291-99
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Chest pain indistinguishable from ischemic
cardiac pain can be caused by GERD
Vakil N et al. Am J Gastroenterol 2006.in press
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0
2
4
6
8
10
12
14
16
oddsratiofordiagnosisat1year
follow
up
GERD
Dyspepsia
Peptic UlcerDisease
Coronary HearDisease
Heart Failure
Ruigomas A et al. Fam Pract 2006; 23:167-74
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Analysis Based on ProGERD study
0
5
1015
20
25
endoscop
y
negatif
Reflux
esophagit
is
A
ll
GERD finding
Prevalenceofnon-ca
rdiacchestpain
(%)
endoscopy
negative
Reflux
esophagitis
All
n : 6215
Jaspersen D A et al. Aliment Pharmacol Ther 2003; 17:1515-20
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Esophageal complications of
Gastroesophageal reflux disease are refluxesophagitis, hemorrhage, sticture, Barretsesophagus and adenocarcinoma
Vakil N et al. Am J Gastroenterol 2006.in press
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57%
31%
12%
0%
10%
20%
30%
40%
50%
60%
Non Erosive Reflux
Disesase
Reflux Esophagitis Barret's
Patient
398 consecutive patients
No alarm symptoms
Sharma Pet al. Gatroenterology 1224 suppl 1 : A-584 (2002)
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the head side of the bed
fat consumption
Stop smoking
Prevent : alcohol, chocolate, coffea, soda Prevent : lie down after eating
Low weight
Prevent : drugs which make LES tonus
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InitialManagement
Long-TermManagement
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EmpiricaltherapySuccessful
Step down to
The Lowest doseThat Controls
symptoms
Continous dailytherapy
Intermittent Coursesof therapy
On-demandtherapy
Dent & Talley, Aliment Pharmacol Ther 2003 (Suppl 1)
Dent et al. Gut 2004 (Suppl 4)
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Patients withpredominant heartburn
23 days out of 7
PPI once daily 4 weeks
H2 BlockerTwice daily continous
PPIOn demand
once daily
PPIOnce daily continous
Relapsing patients are treated for 4 weeksWith double the dose of the medication they
Were randomized to, then back to maintenance
4 weeks
R
Norman Hansen et al. Int J Clin Pract 2005
3 months 6 months
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Meta-analysis of data from six studies showedthat for the diagnosis of GERD in patient withnon-cardiac chest pain :The sensitivity of PPI test was 80% compared
with 19% for placeboThe summary diagnostic odds ratio of the PPItest was 19.35 compared with only 0.61 in theplacebo group
A reduction in non-cardiac chest pain duringPPI therapy is therefore indicative of GERD
Wang WH et al.Arch intern Med 2005;165;1222-8
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GERD can be diagnosed in primary care, basedon troublesome symptoms-reducing thenumber of unnecessary referral for furtherinvestigations
Acid plays a central role in the development of:
Symptomatic Esophageal Syndromes (Typical reflux Syndrome,Reflux Chest Pain Syndromes)
EsophagealSyndromes with Esophageal Injury (such as RefluxEsophagitis, Reflux Stricture, Barretts Esophagus) Extra-Esophageal Syndromes (such as Reflux Cough, Reflux
Laryngitis, Reflux Asthma)
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