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PATOFISIOLOGI
PEPTIC ULCER DISEASE
FITA RAHMAWATI
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DEFINISI
• Acid-related disease: GastritisErosionPeptic ulcer disease (PUD)
• PUD ‡ gastritis dan erosiontype ulcer luka lebih dalam --- muscularis mucosa
Tiga jenis penyebab PUD yang umum terjadi :1. Helicobacteer pylory2. Induksi NSAID3. Stress Ulcer/ SRMD (Stress Related Mucosal
Damage)• Ulcer bisa bersifat acute atau kronis
Acute Ulcer --- SRMD tjd pada px dg kondisi kritis di RSChronic ulcer --- H. pylory dan NSAID padapx rawat jalan
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Peptic Ulcer Disease (PUD) menunjuk pada suatu kelompok gangguan ulcerative pada saluran gastrointestinal bagian atas yang diakibatkan oleh asam dan pepsin
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Helycobacter Pilory
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PENYEBAB PEPTIC ULCER DISEASE
Penyebab lain: • Hypersekresi asam lambung (eg. Zolinger-Ellison
syndrom), perlihatkan gambarnya• Infeksi virus (cytomegalovirus)• Insuffisiensi Vascular ( berkaitan dg caocaine)• Radiasi• Chemoterapy • Genetic subtype --- jarang• Idiopathic
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Zollinger-Ellison syndrome. A large amount of excess acid is produced in response to the overproduction of the hormone gastrin, which in turn is caused by tumors on the pancreas or duodenum. These tumors are usually malignant, must be removed and acid production suppressed to relieve the recurrence of the ulcers.
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PATHOFISIOLOGY
• Gastric dan duodenal ulcer --- ketidakseimbangan antara faktor agresiv (asam lambung dan pepsin) dan mekanisme integritas mucosal (mucosal defense dan perbaikan)
• Kerusakan mukosa berkaitan dg sekresi asam lambung dan pepsin
• HCL disekresi oleh sel parietal --- terdpt reseptor histamin gastrin dan acetylcholin
• Peningkatan as lambung --- px duodenal ulcer, infeksi HP, Px ZES (gastrin-producing tumor)
• Px dg gastric ulcer --- produksi asam lambung normal atau menurun (hypochlorhydria)
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PATHOPHYSIOLOGY
Defensive Mechanism for Gastric Mucous Membrane
Offensive Factors
Acid, Pepsin
NSAIDs
Alcohol
Bilious acid
Free radical
Defensive Factors
Mucus, alkali
PG
membrane factors
Phosphoric lipid
Cell(Cell proliferating
Cell migration )
Small circulation
pH2
pH7
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Patogenesis ulkus peptikum
Asam + Pepsin = mukus + sel-sel
INFLAMASI Faktor-faktor lokal+ = ULKUS
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SEKRESI ASAM• Sel parietal mensekresi asam kedalam lumen lambung
Diaktivasi oleh H+/K+ ATPase (proton pump) mll katalisasi pertukaran H+ intraseluler dengan K+ ekstraseluler
• Sekresi HCl distimulasi oleh Acetylcholine (muscarinic type receptor)
yg dilepaskan dari vagal postganglionGastrin
yg dilepaskan dari G sel di mucosa jika terdapat asam amino dan peptida (dr makanan) di lambung
Histamine (H2 type receptor) Yg dilepaskan dari sel paracrine di dekat parietal sel
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SEKRESI ASAMHistamine's effect on the parietal cell
Mengaktivasi adenylate cyclase, Meningkatkan intracellular cyclic AMP concentrations dan mengaktivasi protein kinase A (PKA). Salah satu efek peningkatan aktivasi PKA phosphorylasi protein cytoskeletal berperan dalam transport pompa H+/K+ ATPase dari cytoplasm menuju plasma membrane.
Ikatan acetylcholine dan gastrin menyebabkan peningkatan konsentrasi intracellular calciumyang bersama c AMP akan mengeluarkan ion hidrogen dari sel parietal menuju lumen lambung
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PATHOFISIOLOGY
• Sekresi asam : jumlah asam yg diekskresi dalam keadaan basal (basal acid output/BAO); setelah stimulasi maksimal (MAO) atau response to a meal
• BAO, MAO dan meal stimulated bervariasi tergantung waktu, kondisi fisiologic , umur, gender dan status kesehatan
• BAO mengikuti cyrcadian rhytm dengan sekresi tinggi pada malam hari dan terendah pada pagi hari
• Pepsinogen (precursor pepsin inaktif) disekresi oleh chief cell yg terdapat pada fundus gastric
• Pepsin diaktivasi pd Ph asam (1,8 – 3,5) , inaktivasi reversible pd PH 4 dan irreversibel pd PH 7
Efek pepsin ---- proteolityk dalam pembentukan ulcer
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PATHOFISIOLOGY
• Mekanisme pertahanan mukosa : mukus dan sekresi bicarbonat, intrinsic epithelial cell defense, dan mucosal blood flow
• Sifat viscous dan netral dari lapisan mucus-bicarbonat melindungi sifat asam dari lumen gastrik
• Perbaikan mucus setelah terjadi kerusakan berkaitan dengan epithelial restitution, pertumbuhan dan regenerasi
• Pemeliharaan integritas mukosa dan perbaikan dimediasi oleh produksi prostaglandin endogen
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COMPLICATION
• Perdarahan saluran cerna bag atasPerdarahan disebabkan oleh erosi kedalam artery dan terjadi pada 10 – 15 % pasien. Perdarahan dapat dapat berupa melena dan hematemesis
• Perforasi kedalam peritoneal cavity terjadi dalam 7% px dg PUD. Perforasi meningkat dengan peningkatan pengg. NSAIDsDitandai nyeri yg tiba-tiba, tajam dan berat, dimulai dari epigastrum dan menyebar ke dalam abdomen.
– Obstruksi terjadi pada 2 % pasien
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Peptic ulcers may lead to emergency situations. Severe abdominal pain with or without evidence of bleeding may indicate a perforation of the ulcer through the stomach or duodenum. Vomiting of a substance that resembles coffee grounds, or the presence of black tarry stools, may indicate serious bleeding.
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GEJALA
• Nyeri abdomen/nyeri ulu hati (sebelah atas perut)
• Mual
• Muntah
• Diare
• Demam
• Lemah
• Hilangnya nafsu makan
• Badan lemah
• Hiccup
• Muntah darah
• Berak darah
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DIAGNOSA
• Gejala menetap
• Test darah lengkap (Hb, WBC, dll)
• Test feces (darah pada feces)
• Endoscopy pada gastrointestinal
atas
• Biopsi pada jaringan lambung
• X-ray pada gastrointestinal atas
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The procedure called gastroscopy involves the placing of an endoscope (a small flexible tube with a camera and light) into the stomach and duodenum to search for abnormalities. Tissue samples may be obtained to check for H. pylori bacteria, a cause of many peptic ulcers. An actively bleeding ulcer may also be cauterized (blood vessels are sealed with a burning tool) during a gastroscopy procedure.