erwin budi cahyono · 2019. 3. 23. · dysmotility h. pylori infection/ inflammation psychosocial...
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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 to full, fullness or nitre, which is suspected come from the abnormality of upper gastro-intestinal tractus.
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Dysmotility
H. pylori infection/
inflammation
Psychosocial
factors
Altered gastric
acid secretion
Gut hypersensitivity
Mechanisms of
dyspepsia
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.
Dyspepsia:
pathogenic mechanisms
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Nature of symptoms
Patient’s degree
of distress
Severity of
symptoms
Alarm features
Assessment
of symptoms
Character
Radiation
Timing, duration
and frequency
Modifying factors
Paré, Can J Gastroenterol 1999; 13: 647–54.
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 to the medication.
chronic dyspepsia
Sigh which is sometimes disappear, sometimes appear, more than two weeks. The sigh is not as tremendous 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 gastric carcinoma (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 of
dyspepsia 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 regions
2. 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 (hebat – komplikasi)
3. Radiologi (foto seri SCBA)
* Kontras tunggal akurasi rendah, sebaiknya kontras ganda
* Gastritis (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 stressChemical Irritant (Alcohol, NSAIDs)Pepsin, Acid
H+
Pepsin, AcidSolubilized mucus
H+
back
diffusion
Surface mucus
cell
Parietal
cell
Gland-type mucus cell
Chief cellShay & Sun’s
balance theory
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• Agresif Factor– Gastric Acid
– Pepsin
– Refluxs bile
– Nicotin
– Alcohol
– Antiinflamation nonsteroid medicine
– Cortikosteroid
– Helicobacter pylori
– Free radical
Agresif Factor Defensif Factor
Defensif Factor
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 gradient
Bicarbonate 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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INFECTION CHRONIC GASTRITIS
Atrophy
Intestinal metaplasia
Lymphoid aggregates
Neutrophil infiltrates
H.pylori Intestinal metaplasia
Neutrophils
Mucus
Mucosa
Muscularis
mucosa
Submucosa
Damaging influences :
Helicobacter pylori
urease
toxins
Gastric acidity
Peptic enzymes
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H.Pylori cover, T.L., et al. :ASM Nwes, 61(!),21,1995
H.Pylori infection
MALT
Lymphoma
Chronic
Superficial
Gastritis
Peptic
Ulcer Disease
Chronic Superficial Gastritis
(Histological Gastritis)
Gastric Cancer
Chronic
Atrophic
Gastritis
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Proposed natural history of Helicobacter
pylori infection in humans
Childhood Old Age
Chronic Active GastritisAcuteGastritis
Environmental
Factors
MultifocalAtrophicGastritis
AntralPredominantGastritis
Gastric Cancer
Lymphoma
Gastric Ulcer
Duodenal Ulcer
Duodenitis
H.pylori
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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 information
Time-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 carcinogens
Inflammatory cell carcinogens
Ascorbic acid -carotene H. pylori
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 asam
a. Anti-muskarinik
b. Antagonis H2 -reseptor (H2RA)
c. Penghambat pompa proton (PPI)
Omeprazole, Rabeprazole, Pantoprazole, Lansoprazole
3. Sitoproteksi
a. Sucralfate
b. Cetraxate
c. Colloidal Bismuth subcitrate
d. Prostaglandin
e. Teprenone
f. Rebamipide
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1. Antasida- netralisir asam lambung, menghilangkan rasa sakit
2. Anti-kholinergik (muskarinik)
- pirenzepin: selektif, 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 efektif: UP, eradikasi Hp, GERD
- > 90% UP sembuh, UD 4 mgg, UG 6 mgg
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Chronic inflammation is a major factor for the pathogenesis of serious gastroduodenaldiseases and in the long term, is one of the most 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 more effectively.
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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 hernia
Hipotension 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) Barrett’sAsthma, 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 of stomach contents causes troublesome symptoms and/ or complicationsSymptoms related to gastro-esophageal reflux become troublesome when they adversly affect an individual’s well-beingReflux symptoms that are not troublesome should not be diagnosed as GERDIn Clinical Practice, the patients should determine if their reflux 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 symptoms
and/or complications
Symptomatic
Syndromes
Extra-Esophageal
SyndromesEsophageal
Syndromes
Proposed
AssociationEstablished
Association
Syndromes with
Esophageal
injury
Typical Reflux
Syndromes
Reflux Chest
Pain Syndromes
Refluks Esophagitis
Reflux Stricture
Barrett’s Esophageus
Adenocarcinoma
Reflux Cough
Reflux Laryngitis
Reflux asthma
Reflux dental Erotion
Pharingitis
Sinusitis
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 troublesome symptoms and/or complication
Vakil N et al. Am J Gastroenterol 2006;101:1900-1920
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“Symptoms related to Gastroesophageal Reflux become troublesome when they adversely affect an individual well-being”
“….mild symptoms occuring 2 or more days a week, or moderate/severe symptoms occuring more 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 should determine if their reflux symptoms are troublesome”
Vakil N et al. Am J Gastroenterol 2006;101:1900-1920
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“The Typical Reflux Syndrome can be diagnosed on the basis of characteristis symptoms, without diagnostic testing”
“Heartburn and regurgitation are the characteristic symptoms of the Typical Reflux Syndrome”
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 patient’s 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 Erosive
Reflux Disease
Treatment Failure
Endoscopy
Empirical Therapy
Complicated
Reflux Disease
Risk Assesment
Alarm Symptoms
~95% of
Patients in
Primary
care
~5%
~35%
~60%
Adapted from Lebenz J et al. World J Gastroenterol.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
od
ds r
ati
o f
or
dia
gn
osis
at
1 y
ear
foll
ow
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
10
15
20
25e
nd
os
co
py
ne
ga
tif
Re
flu
x
es
op
ha
git
is All
GERD finding
Pre
va
len
ce
of
no
n-c
ard
iac
ch
es
t p
ain
(%)
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 reflux esophagitis, hemorrhage, sticture, Barret’s esophagus 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
Pati
en
t
398 consecutive patients
No alarm symptoms
Sharma Pet al. Gatroenterology 1224 suppl 1 : A-584 (2002)
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Life style Modification
Medicamentosa
Operatif Therapy/ Endoscopy
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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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Initial Management
Long-TermManagement
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2x daily PPI + H2RA
2x daily PPI
1x daily PPI
1x daily ½ PPI
Prokinetic + H2RA
Prokinetic
Lifestyle
H2RA
Antacide + lifestyle
Or
Antacide
Highest Efficacy
Lowest Efficacy
*no clear dose-response established
Should be abandoned
Recommended
Current
guidelines
After Dent et al. Gut 1999 (Suppl 2)
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Empirical therapy
Successful
Step down to The Lowest dose
That Controls symptoms
Continous daily therapy
Intermittent Courses of therapy
On-demand therapy
Dent & Talley, Aliment Pharmacol Ther 2003 (Suppl 1)
Dent et al. Gut 2004 (Suppl 4)
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Patients with predominant 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 showed that for the diagnosis of GERD in patient with non-cardiac chest pain :The sensitivity of PPI test was 80% compared with 19% for placeboThe summary diagnostic odds ratio of the PPI test was 19.35 compared with only 0.61 in the placebo group
A reduction in non-cardiac chest pain during PPI therapy is therefore indicative of GERD
Wang WH et al.Arch intern Med 2005;165;1222-8
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A patient-centered approach to diagnosis and management
An evidence-based consensus definition and classification of GERD
A globally applicable definition of GERD
Clarified diagnostic criteria for Barrett’s esophagus
A rational classification for proposed esophageal disorders
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GERD can be diagnosed in primary care, based on troublesome symptoms-reducing the number of unnecessary referral for further investigations
Acid plays a central role in the development of :
Symptomatic Esophageal Syndromes (Typical reflux Syndrome, Reflux Chest Pain Syndromes)
Esophageal Syndromes with Esophageal Injury (such as Reflux Esophagitis, Reflux Stricture, Barrett’s Esophagus)
Extra-Esophageal Syndromes (such as Reflux Cough, Reflux Laryngitis, Reflux Asthma)
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