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Dyspepsia &
Gastroesophageal Reflux
(GER)
Wan NedraBagian Anak FK. Univ YARSI
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1
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1.Peptic ulcer disease
2.GER3.Helicobacter pylory infection
ACID RELATED DISORDERS
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2
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Berupa kumpulan gejala yang non-spesifik
berhubungan dengan saluran pencernaan bagian atas
yang terjadi berulang selama minimal 2 bulan
Chelimsky dan Czinn, 2001
MANIFESTASI KILINIK PUD:
DYSPEPSIA
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3
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Mayor:
Nyeri perut di daerah epigastrium
Muntah berulang ( minimal 3x/bulan)
Minor:
Gejala yg berhubungan dg makan (Anoreksia, BB menurun)
Nyeri perut yg dirasa pd malam hari
Heartburn
Oral Regurgitasi
Neusia kronik
Sendawa berulang
Nyeri perut disekitar umbilikal
Ada riwayat keluarga PUD. Dyspepsia
KRITERIA DIAGNOSTIK DYSPEPSIA
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Evaluasi:- 2 mayoratau
-1 mayor+ 2 minor
-4 minor
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Gejala: Nyeri perut di epigastrium, pada malam hari, regurgitasi,hearburn, BB menurun, hematemesis dan melena
Riwayan Makan:
Makanan berlemak, makanan pedas, caffein, laktose
Penggunaan Obat-obatan:Kortikosteroid, NSAID
Alkohol, tembakau (rokok)
Obat2 yang meransang pengeluaran asam lambung
ANAMNESIS
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5
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Pemeriksaan awal:
Hematologi dg differential count
LFT, Elektrolit
Feses: Parasit
Urinalisis
Pemeriksaan lanjutan:
USG hati dan saluran empedu
Endoskopi
Hydrogen breath test
PEMERIKSAAN LABORATORIUM
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6
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H2 reseptor antagonis:
Cimetidine 2040 mg/ kg/ hari 2 kali / hari maks: 400 mb
Ranitidine 2- 4 mg/ kg/ hari, 2 kali sehari (mak: 150 mg)
Proton Pump Inhibitor
Lansoprazol 0,8 mg/kg/hari
Pmeprazol 0,8 mg/ kg/ hari
Cytoprotective Agents:
Sukralfat 40-80 mg/ kg/ hari, 4 kali sehari ( mak 1 g)
PENGOBATAN
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Gastroesophageal reflux (GER)
the involuntary passage of gastric contents into theesophagus
Regurgitation:
reflux dribbles effortlessly into or out of the mouth
Vomiting:
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forceful expulsion of gastrointestinal contents into the
oesophagus
DEFINISI
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Vomiting
Regurgitation
Gastroesophageal reflux
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Forceful expulsion of gastrointestinal contentsthrough the mouth
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Vomiting
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S.motorik somatik
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S.motorik somatik
Saraf otonom
S. Simpatis
S. Parasimpatis
Saraf enterikN. Vagus
asetil kolinpleksus mienterikus
motilitas sal.cerna
pl. mienterikuspl. submukosa
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Impuls
Chemo-receptor
Trigger Zone
Gastrointestinal tract,
Vomiting center
endogen exogen
Impuls
vomiting
afferen N. Vagus
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Vomiting centre
Chemo-receptor Trigger Zone
Blood Brain Barrier
esophagus
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LES
Fundus
Corpus
Tonus decrease
Antrum Peristaltic decrease
Pylorus
Duodenum
Tonus increase
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Most common in children (> infant)
Confusing the parents
Life-threatening causes of vomiting
Three distinct phases
(1) nausea, (2) retching, (3) emesis
Not preceded in raised intracranial pressure or mechanicalobstruction
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Vomiting
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Age: neonates, infant, child
Gastrointestinal tract: obstruction& non obstruction
Extra-gastrointestinal tract
APPROACH
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Neonates
Atresia esophagus, pylorus stenosis, spitting up
GER, NEC, chalasia, Infection (UTI, OMA, sepsis)
Infantspylorus stenosis, intususeption, hernia
RGE, gastroenteritis, infection, drugs, aerophagia
Children
Intusuception, stricture, gastritis, apendisitis Infection, drugs
ETIOLOGY0 4 / 1 1 / 2 0 1 3
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Scanning gambar HPS
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~ etiology
treat acid and base inbalanced
Drugs:
Domperidone
Metoclopramide
Cisapride
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Therapy
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Gastroesophageal reflux
Just spitting up, or
something more serious ?
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20% general infant population
40% of children consulting a pediatrician
70% of all 4 months old infants
regurgitate at least 1 x/day
25% is considered by the parents as a problem
RGE8% abnormal pH esophagus monitoring
1/3001/1000 severe
(Chouchou, 92; Nelson et al, 1997)
REGURGITATION
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The involuntary passage of gastric contents into theesophagus
saliva, ingested food, drinks, gastric/pancreatic/ biliary secretions
normal phenomenon, +/- accompanying symptoms
physiologic or pathologic reflux
(Carre 1983; Vandenplas, 1992; Orenstein, 1994; Vandenplas, 1993)
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GER
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Physiologic reflux
occurs mainly after meal
does not normally cause symptoms
short duration of reflux episodes
Pathologic reflux
frequent reflux episodes of longer duration
reflux episodes occuring during the day/night
may produce symptoms & inflamation/mucosal injury
GER
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MECHANISMS OF GER
attenuated swallows,dysfunctional peristalsis
Length of LES,
Maturation of LESTLES relaxation
Inadequate
gravitation
delayed gastricemptying,
distension
Deficient or delayedesophageal
acid clearance
Incompetent
LES
delayed gastric emptying
distention
ILES: Lower essophagealsphinter
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RGE
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Acid,Regional blood flow,
tissue prostaglandin E2
permeability to acid
susceptibility to inflamation
Impairment of LES
dysmotility
esophagitis
inflamation
dysfunction
vagal nerve
acid/bile
edema
fibrosis
pylorospasm
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Emesis & regurgitation are the most common
primary GER disease
secondary GER disease
infection, metabolic disorders, & food allergy
stimulation vomiting center in the dorsolateral reticularformation by efferent & afferent impuls
CLINICAL MANIFESTATION GER
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Unusual presentations
~ chronic respiratory disease
apnea, apparent life threatening, SIDS
~ to congenital and/or CNS abnormalities
cerebral palsy, psychomotory retardation
A careful history, observation of feeding, & physicalexamination are mandatory
SYMPTOMS OF GER
(- DISEASE)
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1. a. Parental reassuranceb. Milk-thickening agents (?)
2. Prokinetics
3. Positional adjuvant therapy4. a. H2receptor antagonist
b. Proton pump inhibitors
5. Surgery
TREATMENT
RECOMMENDATIONS
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Frequent small feeding
Decrease the number of transient LES relaxations
Reduced volume cause of distress to infants
Restriction volume in clearly overfed babies
Thickening infants formula
Decrease the frequency & volume of regurgitation
time crying, improves sleep, caloric retention ,
coughing (after feeding)
(Vandenplas, 1994, Borelli, 1997)
REGURGITATION AND
FEEDING
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Thickening formula should be considered as the firststep
Can not be given to breastfed infants
Gastric emptying : Casein > Wheyhydrolysate
FORMULA AND MILK-
THICKENING
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Gastrokinetic actionindirect release of acetylcholine
in the myentericus plexus
Reduces regurgitation
The LES pressure and motility
Esophageal peristalsis, gastric emptying
Increased salivary secretion
protect esophagus via salivary component (bicarbonat buffer)
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Prokinetics
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Sleeping and crying decrease GER
Crying increases abdominal pressure, but also increases LES-P
300prone anti-trendelenburg position
SIDS ?
Beyond the age of SIDS ( > 12 months)
(Orenstein, 1990; Orenstein, 1997; Tobin, 1997)
POSITION, CRYING,
AND REFLUX
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Recent studies report that 45-75% of children withuncontrolled asthma suffer GOR
Prokinetic
GER ~ cough episodes at night in 50% children
remission of resp. symptoms or less anti-asthma medication
(McVeagh, 1987; Orenstein, 1988; Tucci F, 93; Pransky SM, 1992)
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Uncomplicated GER
No investigations
Phase 1 (1-2weeks)
Phase 2 (1-3
weeks)?? reconsider diagnosis of GER
??
pH monitoring
Normal Abnormal
? GOR ? UGIS ?Endoscopy ?
C li t d GER h iti ?
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Complicated GER : esophagitis ?
Endoscopy
Eso > Grade 3?
NO
YES
phase 1 + 2A-R Formula
Cisapride 1-3 mo
phase 1 + 2 + 3 + 4(+ Positional treatment,
H2 / Omeprazole)
control endoscopy
stop phase 3
continue phase
2
Eso > Grade 3 ?
UGIS ??
? Surgery
?
NO
YES
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THANK YOU