dyspepsia diagnosis and management · pdf filey alamat rumah : jl.tegalsari no. 6 rt 09/rw 30,...

CURRICULUM VITAENama                           :  Dr. Sutanto Maduseno, SpPD‐KGEHTempat Lahir : YogyakartaAgama : IslamAlamat Rumah         : Jl.Tegalsari No. 6 RT 09/RW 30, Jl. Palagan Tentara Pelajar Yogyakarta    Alamat kantor : RSUP Dr. Sardjito Pendidikan Terakhir : Sp2 Konsultan Gastroenterohepatologi Status : Menikah

PENDIDIKANSD Jetis Harjo 1 YogyakattaSMPN V YogyakartaSMA III YogyakartaFK UGM YogyakartaSpesialis Penyakit Dalam FK UGMSp2 Konsultan FK UI

RIWAYAT JABATANKepala Poliklinik Penyakit Dalam RSUP Dr. Sardjito Yogyakarta, tahun 2002 ‐ 2009 Wakil Kepala Instalasi Rawat Jalan RSUP Dr Sardjito Yogyakarta. Tahun 2003‐2004.Kepala Instalasi Rawat Jalan RSUP Dr. Sardjito Yogyakarta, tahun 2004 – 2009Ketua tim penguji kesehatan untuk wilayah Propinsi Daerah Istimewa Yogyakarta tahun 2006‐2009Direktur Medik dan Keperawatan RSUP Dr Sardjito, tahun 2009‐sekarang

ORGANISASI PROFESI (Cabang Yogyakarta dan Nasional)Anggota Ikatan Dokter Indonesia (IDI)Pengurus Perhimpunan Spesialis Penyakit Dalam (PAPDI) cabang YogyakartaSeksi Penelitian Pengurus Besar PGI JakartaSeksi Humas Pengurus Besar PPHI JakartaPengurus Ikatan Rematologi Indonesia cabang YogyakartaAnggota Pengurus Cabang PPHI‐PGI‐PEGI Yogyakarta

ORGANISASI SOSIAL DAN PENGHARGAAN‐ Anggota donor darah tetap PMI cabang Kota Yogyakarta sejak tahun 1979, dan saat ini telah menyumbang darah sebanyak 95 kali‐Mendapat penghargaan sebagai dokter puskesmas Teladan Kabupaten Madiun dan Propisi Jawa Timur pada tahun 1987

By Sutanto MadusenoDiv of Gastrohepatology,Depart of Internal 

Medicines, Faculty of Medicine, Gadjah Mada University/Sardjito General Hospital

Yogyakarta

DYSPEPSIADEFINITION :

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 (SCBA)

Dysmotility

H. pyloriinfection/

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

Nature of symptoms

Patient’s degree of distress

Severity of symptoms

Alarm features

Assessment of symptoms

CharacterRadiationTiming, duration and frequencyModifying factors

Paré, Can J Gastroenterol 1999; 13: 647–54.

Dyspepsia: symptom assessment

EthiologyOrganic Dyspepsia :

There is an organ abnormality as ulcer gastro‐duodenal, gastro esofageal refluxs and gastric carcinoma (Talley, 1998)

What is Functional Dyspepsia?Persitent or recurrent pain or discomfort centered in the upper abdomen

12 weeks within previous 12 monthsNo evidence of organic dieseaseNo relation between dyspeptic symptoms and bowel movements (IBS).Exclusion of patients with dominant heartburn

symptoms of dyspepsia vs. diagnosis of functional dyspepsia

Functional Dyspepsia 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)

Dyspepsia SubgroupsDysmotility‐likeUlcer‐likeUnspecified

Rome III Diagnostic Criteria for Functional DyspepsiaFunctional 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

Rome III Diagnostic Criteria for Epigastric Pain SyndromeEpigastric Pain SyndromeAt 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 flatulence3. fulfilling criteria for gallbladder or sphincter of Oddi disorders

Rome III Diagnostic Criteria for Postprandial Distress SyndromePostprandial Distress SyndromeAt least 3 months, with onset at least 6 months previously, of 1 or more of the following:• Bothersome postprandial fullness1. occurring after ordinary-sized meals2. at least several times a week• Early satiation1. that prevents finishing a regular meal2. and occurs at least several times a week

Clasificationacute dyspepsia  (new onset dyspepsia)

Suddenly Sigh with the quality of sigh which is usually more tremendous with a longer response to the medication.

chronic dyspepsiaSigh which is sometimes dissappear, sometimes appear, more than two weeks. The sigh is not as tremendous as acute dyspepsia  with a quick response to the medication.

• Agresif Factor– Gastric Acid– Pepsin– Refluxs bile – Nicotin– Alcohol– Antiinflamation nonsteroid 

medicine– Cortikosteroid– Helicobacter pylori– Free radical

Agresif Factor Defensif Factor

Defensif FactorMucosa blood current (microsirculation)Superficial epithel cellProstaglandinFosfolipid/SurfactansMusinBikarbonatMotilitas

Diagram of the equlibrium theory of integration gastro‐intestinal tractus mucosa especially gastric & duodenum

Proton pumpInhibitor

Gastrin Acetylcholine Histamine

Antagonist H2

H+K+ATPase

H+ Cl-Cl-

(-)

(-)K+

Parietal cell

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

Gastritis; Should we follow symptoms or signs?

Symptom complex� Endoscopic findings� Microscopic inflammations

Clinically appearance of Chronic gastritis

DyspesiaPain pattern : pain‐food‐pain  not always happen, if happen  patognomonis.Pain‐food‐relief  duodeni ulcers.True Diagnosis : endoscopy  biopsy  PA algoritma dyspesia

Presence of symptoms in patients with functional dyspepsia

Tack J, et al.  Gastroenterology 2001;121:526‐35

Gastritis

Endoscopy (Examination Indication)1. A negative result or a doubt result of Radiology 

Examination : too small & too superficial

2. Indication operation of Gastric ulcer  or put aside the vicious

3. Look again if the medical medication is not successed 

4. Determine the source of Hemorrhage

Mechanism of Acid SecretionCephalic phaseGastric phase

Nervus Vagus

Asetilcholine

ECL‐cell

Histamine

Food in Gaster

G‐cell

Gastrin

Parietal Cell

Nervus Vagus

ECL‐cell

G‐cell

Gastrin H+

K+

Clˉ

H+

H+

HCl

Mechanism of Acid SecretionCephalic phaseGastric phase

Asetilcholine

Histamine

Food in Gaster Parietal Cell

Mechanism of Acid SecretionCephalic phaseGastric phase

Nervus Vagus

Asetilcholine

ECL‐cell

Histamine

Food in Gaster

G‐cell

Gastrin

Parietal Cell

Nervus Vagus

ECL‐cell

G‐cell

Gastrin H+

K+

Clˉ

H+

H+

HCl

Mechanism of Acid SecretionCephalic phaseGastric phase

Asetilcholine

Histamine

Food in Gaster Parietal Cell

Algoritm of dyspepsia management in the public 

DYSPEPSIA

AGE < 45 YEARS WITHOUT NATURAL SIGNS

AGE > 45 Years with Natural signs :- vomiting - fever- hematemesis - ictherus- Loose of body WeightThe history of using chronic OAINS The hystory og gastric cancer in the familypasient 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

1. Goal of Pharmacotherapy in dyspepsia

• Control symptoms

• Promote healing

• Prevent complications

• Improve health‐related quality of life

• Avoid Adverse effects of treatment

Pharmacotherapy• Antacids

• Acid Suppression drug

• Prokinetic agent

• Surface agent

DYSPEPSIA

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-Receptora. Cimetidin

dossage 2x (200-400) mg every morning and night or 800 mg at night

b. Ranitidindossage 2x (150-300) mg every morning and night or (300-600) mg at night

c. Famotidindossage 200 mg everyday

3. Motilitas GroupDonperidon 3x1Cisapride 3x (5-10) mg/day

4. Prostaglandin E GroupMisoprostolemprostil

5. Sitoprotectif :Sukralfat, setraksat, Teprenon

6. Others Medicine :Anti anxietyAnti depresiAnti Convulsant

7. If needed :Surgical therapy : vagotomi

Medicine to Control Gastric AcidAntacida

(cheap, low compilance, inefective for gastric ulcers, not consistence in maintaning pH Intragastric, interaction with others drugs, can be used in esofagitis refluxs lightly/moderate)

Antagonist reseptor‐H2(Cimetidine, ranitidine, famotidine)

(consistence in maintaining pH Intragastric 4‐8 hours, less efective at meal stimulated and day time acid secretion, easy to takhifilaksis, inefective to protect gastric ulcers for the OAINS users, can be used in esofagitis refluxs lightly/moderate)

Table 8. The Possibility of  the Side effect that can appear after using medicine which control gastric acid

Drugs to control gastric acid The possibility Side effect

Antagonist histamin2H receptor:

Proton Pomp barrier :

Sitoprotektif drugs :

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.

(Shirakabe, 1995; Brunton, 1996)

Acid supression drugs:• H2RA (H2 Receptor Antagonist)

• PPI (Proton Pump Inhibitor)

CimetidineRanitidineFamotidineNizatidine

OmeprazoleLansoprazolePantoprazoleRabeprazoleEsomeprazole

Trends in Prescribing of Proton Pump Inhibitorsin General Practice in England

“Newer PPIs offer no advantage in terms ofclinical efficacy over established PPIs, areusually more expensive and have lessevidence for long-term safety.”

MeReC Bulletin 2006;16:9-12

Total Expenditure of OTC Antisecretory Therapy, USA, 2003–2006 

Bioav

ailability (%

)

Tolman et al, J Clin Gastroenterol 1997; 24: 65–70.Fitton & Wiseman, Drugs 1996; 51: 460–82.

Hassan‐Alin et al, Gastroenterology 2000; 118: A16.Swan et al., Aliment Pharmacol Ther 1999; 13(Suppl 3): 11–7.

Howden, Clin Pharmacokinet 1991; 20: 38–49.

PPI bioavailability after the first dose

809080706050403020100

Lansoprazole Pantoprazole Esomeprazole Rabeprazole Omeprazole

77

64

52

40

Matur Nuwun