UPPER GI DISORDER 2

PEPTIC ULCER
Bambang Sutopo
FKIK UNJA 10 Sept 2013
 Pendahuluan
Definisi:
Tukak peptik adalah kerusakan pada jaringan
mukosa, submukosa hingga lapisan otot dari
suatu daerah saluran cerna bagian atas yang
langsung berhubungan dengan cairan asam
lambung atau pepsin, dengan diameter jaringan
rusak > 5 mm.
 Pendahuluan

 Ulkus Gaster: nama yang dipakai untuk ulkus

peptikum yang terjadi dilambung.
 Ulkus Duodenum: bila ulkus peptikum terjadi di
duodenum
 Ulkus Esofagus: bila ulkus peptikum terjadi di
esofagus.
 Epidemiologi
 Ulkus peptikum didapati diseluruh dunia.
Menyerang pria > wanita.
 Pada kelompok geriatri, prevalensi meningkat.
 Klinis, ulkus duodeni lebih banyak ditemui. Tapi
pd autopsi, jumlah penderita ulkus gaster dan
ulkus duodeni sama.
 Epidemiologi
Faktor2 yg bisa menyebabkan ulkus:
 Kuman Helicobacter pylori.
 Pemakaian obat2 gol. NSAID (Non Steroid Anti
Inflamatory Drug).
 Smoking.
 Penyakit2 lain.
 Stress dan faktor psikologik
 Lain2: Diet, Alkohol, Kortikosteroid.
 Helicobacter pylori dan ulkus
peptikum
 Telah terbukti kuman2 Helicobacter pylori (H
pylori) sebagai penyebab utama ulkus peptikum.
 NSAID dan ulkus peptikum
 NSAID tercatat sebagai faktor penyebab ulkus
nomer 2 setelah H pylori.
 Merokok dan ulkus peptikum
 Secara statistik didapati prevalensi penderita
ulkus diantara smoker lebih tinggi ketimbang
non smoker.
 Penyakit2 berkaitan dg ulkus
peptikum
 Sindrom Zollinger –Ellison (Gastrinoma)
 Penyakit Paru Obstruktif Kronik (PPOK)
 Gagal ginjal kronik
 Cirrhosis hepatis
 Stress dan ulkus peptikum
 Stress akut: pada operasi besar, luka bakar dll
 Stress kronis: stress yang berkepanjangan.
 Hal2 lain yg berkaitan dg ulkus
peptikum
 Kortikosteroid
 Alkohol
 Diet
PATHOPHYSIOLOGY

Schwarst 1910
“ No Acid No Ulcer “
 History of Acid

1910
Dictum Schwartz
“No Acid – No Ulcer”
 PATOFISIOLOGI
AGRESIF
1. Endogen
2. Eksogen

DEFENSIF
Mukosa gastroduodenal
Shay and Sun : Balance Theory 1974
Gangguan Keseimbangan antara
Faktor Agresif dengan Faktor Defensif
Shay and Sun’s Balance Theory
etiology of peptic ulcer
b

ulcer
no
ulcer

aggressive factors

HCL and pepsin secretion

vagal phase
O (cephalic nervous)
antral phase
mucosal defensive factors
(hormonal)
cephalic humoral phase
mucosal resistance (adrenal)
Mucus parietal cell mass
Local mucosal blood flow mucosal trauma
Duodenal “Brake”
AGRESIF
Warren
and
Marshall
1983

Helicobacter pylori (Hp)

“ No Hp No Ulcer”
 Natural history of H.pylori infection
H.pylori infection
weeks to months

Chronic superficial gastritis

(Histological gastritis)
years

Peptic Chronic MALT Chronic

ulcer superficial lymphoma atrophic
disease gastritis gastritis

Gastric
cancer
H.pylori Cover,T.L.,et al.:ASM News, 61(1),21,1995
Proposed natural history of Helicobacter pylori infection
in humans
H. pylori infection

?
Virulence
Host
Environment
 Patofisiologi Tukak Peptik
 Pertahanan mukosa VS Faktor agresif.
 Patofisiologi ulkus esofagus
 Patofisiologi ulkus gaster
 Patofisiologi ulkus duodenum
 Patofisiologi tukak peptik
Pertahanan mukosa:
 Mukosa esofagus terdiri dari epitel
skuamosa, lebih kuat menahan goresan dari bahan2 yang
melewati. Waktu kontak dg bahan2 tsb juga sebentar.
 Mukosa gaster juga terdiri dari epitel yang kedap (tight
epithelum), relatif lebih kuat.
 Mukosa duodenum relatif paling lemah, lebih gampang
cedera.
 Patofisiologi tukak peptik
Patofisiologi ulkus esofagus
 GERD (Gastro Esophageal Reflux Disease)

 Esofagitis erosif

 Barrett’s esofagus

 Ulkus esofagus

 Karsinoma esofagus
 Patofisiologi tukak peptik
Patofisiologi ulkus gaster:
 Infeksi H pylori dan akibat pemakaian NSAID
menempati urutan pertama penyebab ulkus
gaster (90%)
 Patofisiologi tukak peptik
Patofisiologi ulkus duodenum:
 Mukosa duodenum relatif paling lemah
dibanding gaster dan esofagus.
 Terjadinya ulkus duodeni akibat ketidak
seimbangan faktor yang melindungi dan faktor
yang merusak.
 Manifestasi klinik
 Nyeri abdomen
 Komplikasi ulkus
 Diagnosa banding
 Manifestasi Klinik
Nyeri abdomen, yang sifatnya:
 Seperti rasa terbakar

 Terlokalisir di epigastrium, tidak menjalar,

timbul 2-3 jam setelah makan atau pada malam
hari.
 Rasa sakit hilang setelah makan atau hilang
dengan antacid.
 Manifestasi klinik
Komplikasi ulkus peptikum:
 Perdarahan

 Perforasi

 Obstruksi
 Manifestasi klinik
Diagnosa banding:
 Non Ulcer Dispepsia.

 Kelainan/penyakit diluar saluran cerna.

 Differential Diagnosis
 Neoplasm of the stomach
 Pancreatitis
 Pancreatic cancer
 Diverticulitis
 Nonulcer dyspepsia (also called functional
dyspepsia)
 Cholecystitis
 Gastritis
 GERD
 MI—not to be missed if having chest pain
 Diagnosis
 Berdasar symptom dan sign
 Anamnesis.
 Pemeriksaan fisik.
 Pemeriksaan Laboratorium.

 Radiologi.

 Endoskopi.
 Diagnosis ulkus peptikum
 Laboratorium
 Darah rutin: mengetahui ada anemia/tidak
 Pemeriksaan tinja, tes Benzidin: mengetahui ada
perdarahan SCBA/tidak.
 Diagnosis ulkus peptikum
Radiografi:
 Foto polos abdomen

 Foto Barium
 Diagnosis ulkus peptikum
 Endoskopi: Diagnostik maupun terapeutik.
 Keunggulan endoskopi: bisa melakukan biopsi
dan diagnostik secara PA.
 Sekarang: sudah ada tehnik endoscopic ultraso
nography
TREATMENT OF PUD

 RELIEFSYMPTOMS
 PREVENT COMPLICATIONS

 HEALING ULCER.

 PREVENT RELAPS
 Terapi ulkus peptikum
 Terapi terhadap Helicobacter pylori.
 Terapi terhadap asam lambungnya.
 Terapi dan pencegahan ulkus akibat NSAID.
 Terapi pencegahan ulkus kambuh dan
komplikasi.
 Terapi ulkus peptikum
Terhadap H pylori; kombinasi 3 agen:
 Proton pump inhibitor: omeprazol, lansoprazol,
pantoprazol, rabeprazol.
 Klaritromisin

 Metronidazol atau amoxillin.

 Treatment Plan: H. Pylori
 Medications: Triple therapy for 14 days is considered
the treatment of choice.
 Proton Pump Inhibitor + clarithromycin and amoxicillin
 Omeprazole (Prilosec): 20 mg PO bid for 14 d or
Lansoprazole (Prevacid): 30 mg PO bid for 14 d or
Rabeprazole (Aciphex): 20 mg PO bid for 14 d or
Esomeprazole (Nexium): 40 mg PO qd for 14 d plus
Clarithromycin (Biaxin): 500 mg PO bid for 14 and
Amoxicillin (Amoxil): 1 g PO bid for 14 d
 Can substitute Flagyl 500 mg PO bid for 14 d if allergic to PCN
 In the setting of an active ulcer, continue qd proton pump
inhibitor therapy for additional 2 weeks.
 Goal: complete elimination of H. Pylori. Once
achieved reinfection rates are low. Compliance!
 Terapi ulkus peptikum
Terhadap asam lambungnya:
 Golongan Antacida:
 Golongan H2 blocker: Ranitidin, famotidin.
 Golongan Proton pump inhibitor: Omeprazol,
lansoprazol, pantoprazol, rabeprazol.
 Golongan Sukralfat:
 Golongan Prostaglandin Analog: Mesoprostol
 Treatment Plan: Not H. Pylori
 Medications—treat with Proton Pump
Inhibitors or H2 receptor antagonists to
assist ulcer healing
 H2: cimetidin, ranitidin and famotidin for
up to 8 weeks
 PPI: omeprazol, lansoprazol,
essomeprazol for 4-8 weeks.
 Lifestyle Changes
 Discontinue NSAIDs and use Acetaminophen for
pain control if possible.
 Acid suppression--Antacids
 Smoking cessation
 No dietary restrictions unless certain foods are
associated with problems.
 Alcohol in moderation
 Men under 65: 2 drinks/day

 Men over 65 and all women: 1 drink/day

 Stress reduction
 Management of NSAID-induced
peptic ulcer disease
Discontinue use of NSAIDs or substitute with less
toxic agents
 Low-toxicity NSAIDs or COX-2
inhibitors
Suppress acid secretion
 Normal-dose PPI therapy
 (High-dose H2RA therapy )
Use mucosal protectants
 Misoprostol (substantial side-effects,
abortifacient)
 Rebamipide
Seager & Hawkey, BMJ 2001; 323: 1236–9.
 ETC. Silverstein et al., Ann Intern Med 1995; 123: 241–9.
Graham et al., Ann Intern Med 1993; 119: 257–62.
Yeomans et al., N Engl J Med 1998; 338: 719–26.
 Prevention
 Consider prophylactic therapy for the following patients:
 Pts with NSAID-induced ulcers who require daily NSAID
therapy
 Pts older than 60 years
 Pts with a history of PUD or a complication such as GI
bleeding
 Pts taking steroids or anticoagulants or patients with
significant comorbid medical illnesses
 Prophylactic regimens that have been shown to dramatically
reduce the risk of NSAID-induced gastric and duodenal
ulcers include the use of a prostaglandin analogue or a
proton pump inhibitor.
 Misoprostol (Cytotec) 100-200 mcg PO 4 times per day
 Omeprazole (Prilosec) 20-40 mg PO every day
 Lansoprazole (Prevacid) 15-30 mg PO every day
 Complications

 Perforation & Penetration—into pancreas,

liver and retroperitoneal space
 Peritonitis
 Bowel obstruction, Gastric outflow
obstruction, & Pyloric stenosis
 Bleeding--occurs in 25% to 33% of cases
and accounts for 25% of ulcer deaths.
 Gastric CA
 Surgery
 People who do not respond to medication, or who
develop complications:
 Vagotomy - cutting the vagus nerve to interrupt
messages sent from the brain to the stomach to reducing
acid secretion.
 Antrectomy - remove the lower part of the stomach
(antrum), which produces a hormone that stimulates the
stomach to secrete digestive juices. A vagotomy is
usually done in conjunction with an antrectomy.
 Pyloroplasty - the opening into the duodenum and small
intestine (pylorus) are enlarged, enabling contents to
pass more freely from the stomach. May be performed
along with a vagotomy.