dr Shahrul Rahman, Sp.

PD

Departemen Ilmu Penyakit Dalam

Fakultas Kedokteran
Universitas Muhammadiyah Sumatera Utara

TUKAK PEPTIK
(PUD)mukosa sal. cerna yang luas akibat
Kelainan
asam dan pepsin
LOKASI : LAMBUNG, DUODENUM
Incidents in Western Countries : Female 4 15 % &
Male 10 15 %
TD (MENURUN), TL(MENINGKAT)
Upper GI endoscopy in Cipto Mangunkusumo Hospital:
The incidence of Peptic Ulcer: 6,93 7,10%;
Duodenal Ulcer: Gastric Ulcer = 2:1
EPIDEMIOLOGI PUD BERVARIASI

PATOGENES
E
1. SCHWARTZ
NO ACID NO ULCER 1910
2. SHAY AND SUN : KETIDAKSEIMBANGAN FAKTOR
AGRESIF (asam pepsin) & DEFENSIF (mukus bile,
aliran darah PG berkurang, regenerasi sel epitel).
3. WARREN AND MARSHALL 1983 NO HP NO
ULCER
TL : 60-80% HP, 25% OAINS, 5% SZE
TD : 90-95% HP, 5% OAINS, 5% SZE

MIKROBIOLOGI

Hp

batang gram (-).

berbentuk spiral.
mempunyai banyak flagel aktif.
penghasil urea yang kuat.

Gambar 1. Helicobacter Pylori.

TRANSMISI
Rute faecal oral

terjadi pada masa kanak-kanak

Dibuktikan dari

kultur dan PCR feses Hp (+).

prevalensi hepatitis A // infeksi

Terutama di negara berkembang.
Rute oral oral
Regurgitasi.
PCR air liur dan plak gigi.
Afrika memamah.
Pemakaian sendok secara bersama sama.
Negara maju ciuman.
Rute gastro - oral
Melalui muntahan jalur utama.

Pathogenesis of NSAID-induced
ulcers
PROTECTIVE
FACTORS

AGGRESSIVE FACTORS

Prostaglandins

Acid + pepsin

H. pylori

Mucus layer
Bicarbonate
Surface
epithelial
cells
Mucosal blood
supply
Seager & Hawkey, BMJ 2001; 323: 12369.

Pathogenesis of NSAID-induced
ulcers
PROTECTIVE
FACTORS

AGGRESSIVE FACTORS

Prostaglandins

NSAIDs

Acid + pepsin

H. pylori

Mucus layer
Bicarbonate

Surface
epithelial
cells
Mucosal blood
supply

Seager & Hawkey, BMJ 2001; 323: 12369.

DIAGNOS
A KLINIS : NYERI EPIGASTRIUM ATAU DYSPEPSIA

GASTRIC ULCER
- Uncommon before 40
years of age
- Pain often in increased
by food intake, relieved
by fasting
- Acid secretion normal
- Weight loss possible
- Haematemesis may occur

* DUODENAL ULCER
- Occur between 25 and 55 years
- Pain temporarily relieved
by food intake and antacids
pain is often nocturnal
- Acid hypersecretion
- No weight loss
- Melaena may occur

PD & LAB . BATAS NORMAL

PEMERIKSAAN PENUNJANG Radiologi: OMDF
(CRATER NICHE TL),
ENDOSKOPI : OEDEM , ERITEMA, EROSI, ULKUS ( SIDNEY
CLASSIFICATION)
H. PYLORI TESTING

POTENTIAL COMPLICATIONS OF
PUD

HAEMORRHAGE
- CAUSED BY ULCER ERODING BLOOD VESSEL WALL ; MAY
RESULT IN DEATH

PERFORATION

- CAUSES SUDDEN INTENSE PAIN AS GUT CONTENTS

ESCAPE
INTO ABDOMINAL CAVITY ; REQUIRES
HOSPITALISATION
AND USUALLY SURGERY

OBSTRUCTION

- SCARRING MAY BLOCK STOMACH OUTLET, PREVENTING

FOOD PASSAGE. PATIENTS EXPERIANCE VOMITING AND WEIGHT
LOSS;REQUIRES HOSPITALISATION AND USUALLY
SURGERY

PENATALAKSANAAN
TANPA ATAU DENGAN KOMPLIKASI
H. pylori eradication is essential in H.
Pylori - positive patients
NSAIDs should be discontinued or
reduced, if possible
PPIs are the most effective agents for
acid
suppression and the most
appropriate
first - line therapy

DENGAN KOMPLIKASI
(SURGICAL ULCER)
Total gastrectomy
Antrectomy
Vagotomy
Pyloroplasty
Close perforation
Billroth I and II

TUJUAN
MENGURANGI / MENGHILANGKAN KELUHAN
PENGOBATAN

PENYEMBUHAN LUKA

MENCEGAH TERJADINYA KOMPLIKASI

MENCEGAH TERJADINYA KEKAMBUHAN

TL > TD LAMA TERAPI

TL 6 MG,TD 4 MG,80-90 % SEMBUH!

A. NON MEDIKAMEN GAYA HIDUP ( TENANG, BERGAIRAH, PUNYA

HOBBY /

KERJA, TIDAK KAKU DALAM

DENGAN WAJAR ), DIET

PERGAULAN, STRESS

SEIMBANG, CABE MERANGSANG ?,

INTOLERANSI MAKANAN, ROKOK

(PJK,PPOM, SKRESI BIKARBONAT,

REFLUKS DUEDENO GASTER,

KESEMBUHAN TERLAMBAT. ALKOHOL,

ASAM, COCACOLA, BIR, KOPI,

ULSEROGENIK

B. MEDIKAMEN RAWAT JALAN KALAU PERLU RAWAT INAP

(KESEMBUHAN ,
LAMBUNG , ANALGETIKA

JAM ISTIRAHAT , REFLUKS , STRESS , ASAM

MEDIKAMEN
ANTASID (Al(OH)3 & Mg(OH)2
ANTAGONIST RESEPTOR-H2(ARH-2)
MEMBLOKIR HISTAMIN PADA PARIETAL SEL

Simetidin, ranitidin,famotidin, roxatidine,

nizatidine
PENGHAMBAT POMPA PROTON (PPI-PPP)
MENGIKAT POMPA PROTON DARI SEL PARITEL
MENGHAMBAT SEKRESI IONHIDROGEN KE DALAM LUMEN LAMBUNG

Omeprazole, lanzoprazole, panthoprazole, rabeprazole &

esomeprazole
OBAT SITOPRETEKTIF, Sucralfate, Cetraxate, Terpenone
REBAPIMIDE
Gastro-protective ( prostaglandin inducer, anti inflammatory
modulator dan anti free radical/scavengers )
PROSTAGLANDIN, Analog misoprostol

PENATALAKSANAAN INFEKSI H.
PYLORI

SANGAT DIANJURKAN : tukak duodeni, tukak lambung,

paska
reseksi KLD, limfoma MALT.
DIANJURKAN : dispepsia tipe ulkus, gastritis kronik aktif,
gastropati OAINS, gastritis erosiv, gastritis hipertrofik
TIDAK DIANJURKAN pasien asimptomatik

REGIMEN TERAPI
TERAPI DUAL : PPI & ANTIBIOTIK
TERAPI TRIPEL : PPI + AMOKSILIN + KLARITROMISIN
PPI + METRONIDAZOL + KLARITROMISIN
PPI + METRONIDAZOL + TETRASIKLIN
TERAPI KUADRIPEL
BISMUTH + PPI + AMOKSISILIN + KLARITROMISIN

Consensus of The Treatment H Pylori

Infection
First Line Therapy
For H Pylori Eradication
(Maastrich
III-2005)
PPI- Clarithromycin Amoxicillin or metronidazole therapy remains the recommended
first line Therapy In populations with less than 15-20% clarithromycin resistance
Prevalence, in population in Less than 40% Metronidazole resistance prevalence
PPI clarithromycin - metronidazole is preferable
Quadriple therapies are alternative first line therapy

In case of failure
Second line therapy
Bismuth based quadruple therapies remain the best second line therapy, if available,
if not, PPI Amoxicillin or tetracycline and metronidazole are recommended

Subsequent failures rescue therapy

The rescue therapy should be based on antimicrobial susceptibility testing