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8/18/2019 Gastritis and Peptic Ulcer Disease
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Gastritis akutGastritis akut(Erosif/Hemorrhagik)(Erosif/Hemorrhagik)
#mumnya disebabkan oleh#mumnya disebabkan oleh $$%n&ury' pada mukosa lambung karena NA%%n&ury' pada mukosa lambung karena NA%
dengan mengurangi produksi prostaglandindengan mengurangi produksi prostaglandin
pada lambung dan duodenum pada lambung dan duodenum *onsumsi alkohol*onsumsi alkohol
$$tress' akibat +edera kepala lukabakartress' akibat +edera kepala lukabakar
sepsis pembedahansepsis pembedahan
,ipertensi ortal (portal gastropathy),ipertensi ortal (portal gastropathy)
enyebab lain:enyebab lain: Terminum bahan-bahan korosi/kaustikausti+Terminum bahan-bahan korosi/kaustikausti+
ingestioningestion
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Gastritis kronikGastritis kronik Nonerosif/nonspesifik Nonerosif/nonspesifik
Gastritis infeksiosa Type B: H PyloriGastritis infeksiosa Type B: H Pylori Mengenai antrum dan corpus gaster Mengenai antrum dan corpus gaster Kebanyakan asimptomatik Kebanyakan asimptomatik Ada hubungan kuat dengan penyakit ulkus peptikum Ada hubungan kuat dengan penyakit ulkus peptikum
Risiko adenokarsinoma dan limfoma !" kali lipatRisiko adenokarsinoma dan limfoma !" kali lipat Gastritis autoimmune Type A: AnemiaGastritis autoimmune Type A: Anemia pernisiosa pernisiosa
Biasanya mengenai corpus dan fundus# mempengaruhiBiasanya mengenai corpus dan fundus# mempengaruhisel parietal$sel parietal$
Anemia pernisiosa disebabkan oleh gangguan Anemia pernisiosa disebabkan oleh gangguanabsorbsi %itamin B& karena tidak adanya faktorabsorbsi %itamin B& karena tidak adanya faktorintrinsik dari sel parietal dan berkurangnyaintrinsik dari sel parietal dan berkurangnya
produksi asam produksi asam Risiko adenokarsinoma bertambahRisiko adenokarsinoma bertambah
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Bentuk!bentuk khususGastritis 'nfeksiosa (Gastritis flegmonosa atau
)necroti*ing gastritis+, Reseksi lambung emergensi# dan pengobatandengan antibiotika
-M.# candida (/amur, pada penderita+immunocompromised+
Gastritis eosinofilik )Giant -ell gastritis+ (Menetrier0sdisease atau gastropati hipertrofik,
Gastritis limfositik
Gastritis granulomatosa Tuberkulosis 1yphilis 2amur 1arkoidosis -rohn0s disease
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Ge/ala!ge/ala Gastritis
Gambaran klinis gastritis umumnya lebih mencerminkan sindroma yang mendasari dibandingcedera gaster sendiri
Akut: 3ispepsia dan nyeri abdomen Ketidakenakan daerah epigastrik Kadang!kadang mual ( nausea, dan muntah (%omitus, 4yeri kepala# sali%asi berlebihan# flatus
Kronik:
Ge/ala tak khas# mungkin hanya discomfort abdominalsa/a$
Tanda!tanda: (tidak selalu ada, Hematemesis 4yeri tekan abdomen (abdominal tenderness,
Kembung (Bloating, Muntah
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Gastritis
5aboratorium: 1tandar emas (gold standard, adalah pemeriksan
endoskopi6biopsi 7rea breath test untuk mendeteksi H$ pylori Pemeriksaan khusus untuk kondisi yang mendasari# misalnya pemeriksaan kadar %it B&
dan P35 untuk anemia perniciosa 3iagnosis differensial:
&$ 7lkus peptikum $ Gastroparesis 8$ Karsinoma lambung 9$ GR3 ;$ Pankreatitis "$ 5imfoma
Pengobatan Hilangkan irritant radikasi H$ pylori Antasida dan H blocker
Hindari rokok dan alkohol
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7lkus peptikum
7lkus peptikum atau Peptic 7lcer 3isease7lkus peptikum atau Peptic 7lcer 3isease(P73, adalah penyakit ulkus yang terdapat(P73, adalah penyakit ulkus yang terdapat
pada saluran cerna bagian atas (lambung dan pada saluran cerna bagian atas (lambung dan
duodenum, ulcus %entriculi# ulcusduodenum, ulcus %entriculi# ulcusduodeniduodeni
Kerusakan mukosa lambung atau duodenum Kerusakan mukosa lambung atau duodenum meluas sampai tunica muscularis mucosae# meluas sampai tunica muscularis mucosae#
biasanya sedalam ; mm!& cmbiasanya sedalam ; mm!& cm
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• Perbandingan frekuensi pria dengan
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1pektrum penyakit ini luas# mulai daricedera ringan mukosa sampai ulserasi yangtampak /elas
Ge/alanya ber%ariasi dan tidak selalu ada
hubungan dengan beratnya kerusakan/aringan$
1aat ini pre%alensi ulkus peptikum kira!kira &!= penduduk
&>= penduduk pernah mengalami penyakit
ulkus peptikum sepan/ang hidupnya 7lkus %entrikuli dan ulkus duodenicenderung kambuh pada lokasi yang sama$
Perdarahan rekurens dapat ter/adi pada
;>= penderita$
7lkus peptikum
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Ulkus Duodeni vs. Ulkusventrikuli
Ulkus Duodeni Produksi asam meningkat
H$ pylori
Keluhan berkurangbila dimasuki
makanan danbiasanya penderitaterbangun pada
tengah malam akibatsakitnya
Ulkus ventrikuli Produksi asamnormal atau
berkurang Resistensi mukaberkurang
H$ pylori 41A'31
Keluhan makin
memburuk dengan makanan
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?nset sering ter/adi
pada usia ; !;; th Tak pernah men/adiganas
Kebanyakan ulkusterdapat di bulbusduodeni atau postbulbus$
7lkus yang terletak didistal bulbus duodeni mungkin suatu sindroma @ollinger!llison7lcers$
Pria banding
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@ollinger!llison 1yndrome
#lkus yangberhubungan
dengan indroma ollinger-0llisondisebabkan olehgastrin-releasing
islet +ell tumors(gastrinoma)dianggap &ugasebagai ulkus
peptikum.
http://upload.wikimedia.org/wikipedia/commons/5/54/ZES_endo.jpg
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@ollinger!llison 1yndrome
1erupakan tumor pankreas yang mensekresigastrin ( Gastrinoma)
"iasanya terdapat di pankreas tetapi dapat &ugadi duodenum hati dan paru
23-456 terdapat di bulbus duodenum apat di+urigai sindroma 0 :
#lkus multipel atau rekurens #lkus terletak di postbulbus atau &e&unum
#lkus disertai dengan diare *adar gastrin serum meningkat (hanyadiperiksa bila di+urigai sindroma 0)
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tiologi ulkus peptikum
&$ Penyebab pertama 'nfeksi Helicobacter pylori(H$ pylori, :
a$ Terdapat pada C>!D;= ulkus peptikum$
b$ Pengobatan terhadap H$ pylori
meningkatkan angka kesembuhan ulkus dan menurunkan angka kekambuhan$
$ Penyebab kedua 41A'31: ?bat!obat ini menghambat prostaglandin yang pada keadaan
normal merangsang produksi sekresi mukus danbikarbonat
a$ 3apat menyebabkan ulkus %entrikuli danduodeni
b$ Penyebab kebanyakan ulkus non H$ pylori
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8$ Keadaan hipersekresi
a$ Gastrinoma (@ollinger!llison 1yndrome,b$ Multiple endocrine neoplasia (M4!&,c$ 1ystemic mastocytosis (mast cells
infiltrate intestinal
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3efensi%eforces Mucus BicarbonateProstaglandins
pithelialregeneration
Aggressi%eforces Gastric acid 3igesti%een*ymes
Patogenesis PUD ada hubungannyadengan ketidakseimbangan antara faktor protektif nomal dan faktor
“injury”
!
7lcer
4o 7lcer 4ormal
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Ulkus dapat ter"adi akibat# $gresi meningkat
%nfeksi H. p&lori
N!$%D!
'okok dll
Atau
Pertahanan terganggu
'schemia 'nhibisi Prostaglandin (41A'31,
Pengosongan lambung terlambat (3elayedgastric emptying,
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fek merugikan merokok
&$ Mempengaruhi aksi obat Hantagonists
$ Meningkatkan la/u pengosonganlambung
8$ Meningkatkan refluks duodenogastrik
9$ Menurunkan sekresi bikarbonat
;$ Menurunkan aliran darah mukosa
"$ Menekan sintesis prostaglandin mukosa gaster
7lkus peptikum
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Ge/ala dan Tanda P73
Nyeri epigastrik 7asa terbakar
Timbul 8-9 &am sesudahmakan
"erkurang denganmakanan
apat ter&adi malamhari
Nyeri dapat terasasampai punggung ataubahu bila ada perorasi
Nausea
omitus
ispepsia *embung/rasa penuh
,eartburn/pirosis 7asa tak enak di dada
(hest is+omort) Anoreksia
"erat badan turun ada ulkus ;entrikuli "erat badan naik
ada ulkus duodeni
,ematemesis atau
melena *arena perdarahansaluran +erna
"ila berat/prouse hematoke
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Pengelolaan P73
4on!Earmakologik
Perubahan 3iet 1top rokok
?bat!obat yang memperberat penyakit dihentikan
Earmakologik Menghambat sekresi asam
Menetralkan asam lambung
Meningkatkan proteksi mukosa lambung
Antibiotika bila perlu
Terapi Maintenance
Pre%ensi dengan colloid bismuth Pemberian H blockers malam hari
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H5'-?BA-TR pylori
Helicobacter pylori (H$ pylori, is a gram negati%espiral!shaped bacillus
found in the gastric mucouslayer or adherent to theepithelial lining of thestomach$
H$ pylori causes more thanD>= of duodenal ulcers and
up to >= of gastric
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Heliobater p&lori
't is not kno
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H l i i f ti
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H. p&lori infetion
Before this bacterium
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H$ Pylori infection
Fhen acid suppression is remo%ed#the ma/ority of ulcers#
particularly those caused by H$
pylori# recur$
1ince
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Most persons
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H.p&lori diagnostie,aminations !erologial tests that measure specific H$ pylori
'gG antibodies can determine if a person has beeninfected$ The sensiti%ity and specificity of these assays around
>=
-eal $ntigen $ssa&
Urea reath test 'n this test# the patient is gi%en either &8-! or &9-!
labeled urea to drink$
H$ pylori metaboli*es the urea rapidly# and thelabeled carbon is absorbed$
This labeled carbon can then be measured as -? in the patients eIpired breath to determine
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Urea reath test 'n this test# the patient is gi%eneither &8-! or &9-!labeled urea todrink$
H$ pylori metaboli*es the urearapidly# and the labeled carbon isabsorbed$
This labeled carbon can then be measured as -? in the patientseIpired breath to determine
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Diagnosis H. &lori in eptiUler Disease
Upper endosop& (esophagogastroduodenal) isonsidered the referene method
of diagnosis.
Peptic 7lcer 3isease
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Peptic 7lcer 3isease :Treatment Pharmacological Therapy
'nhibition of acid
H blockers
Antacids
Proton pump inhibitors
Anticholinergics
Prostaglandins
Augmentation protection
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Peptic 7lcer 3isease :Treatment Antacids (magnesium# aluminum# J calcium based,
cause diarrhea
Moderate to high doses of H blockers result in
impro%ed healing rates 7sed & hr P- J H1 for "!
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Peptic 7lcer 3isease :Treatment Proton Pump 'nhibitors:
'nhibit the H#K!ATPase pump
Healing rate >!&>>=
?mepra*ole# lansopra*ole# rabepra*ole#
pantopra*ole# meromepra*ole
Anticholinergics: reduce acid by ;>= andcause blurred %ision
pupil dilation# consider patient0soccupation or dri%ing restriction
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Peptic 7lcer 3isease :Treatment
Prostaglandins (3o not use in pregnancy, 'nhibit the parietal cell cyclic AMPfunction in response to histamine
Healing rate are eual to H blockers Primary role is to be used as a prophylactic agent to pre%ent 41A'3induced ulcers$ 4ot used as a primarytherapy
Misoprostol (-ytotec,
1ucralfate : its action is unkno
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Peptic 7lcer 3isease :Treatment Regiment for H$
pylori urrent therap& for H. p&lori infetiononsists of 01 da&s to 2 3eeks of one or t3oeffetive antibiotis4 amo,iillin4
tetra&line not to be used for hildren 502 &rs metronida6ole4 or larithrom&in4
lus either ranitidine bismuth itrate (H2 bloker)4 bismuth subsali&late (pepto7bismol)4 or proton pump inhibitor.
Peptic 7lcer 3isease :
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Peptic 7lcer 3isease :Treatment Regiment for H$
pylori Acid suppression by the H blocker or proton pump inhibitor in con/unction
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-urrently# eight H$ pylori treatmentregimens are appro%ed by the Eood and 3rug Administration (E3A, ho
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Peptic 7lcer 3isease :Treatment Regiment for H$ pylori(E3A Appro%ed,
&$ ?mepra*ole 9> mg L3 clarithromycin ;>> mg T'3 I mg L3 I > mgB'3 clarithromycin ;>> mg T'3 I > mg B'3 I > mg L'3N I > mg T'3 I &> days
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8ong7term onse9uenes of H. p&lori infetion+
Recent studies ha%e sho
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UPPERUPPERGASTROINTESTINALGASTROINTESTINAL
HEMORRHAGEHEMORRHAGE
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Incidence %Common causes
Peptic Ulcer 45
Dudenal ulcer
Gastric ulcer
Esophageal varices 20
Gastritis 20
Mallory-eiss
syndro!e
"0
Uncommon causes 5
Gastric #arcino!a
Esophagitis
Pancreatitis
$e!oilia
Duodenal
diverticulu!
CAUSES
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Gastric Ulcer Duodenal Ulcer #a-&to!ach
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Esophageal varicesGastritis
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Mallory-eiss 'ear
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• Hematemesis
•
.omiting of blood is common
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• $e!atoche(ia$e!atoche(ia
• It is defned as passage o bright-red blood romthe ractum.
• Common in bleeding rom Colon, Rectum andAnus.
• In case o brisk bleeding in the Upper GIT, rightred blood ma! come out unchanged in the stool.
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Initial assess!ent and !anage!ent goals"• Assessment o the status o the circulator!
s!stem and replace blood loss as necessar!.
•#etermine the amount and rate o bleeding.•$lo% or stop the bleeding b! ice-%ater la&age
•#isco&er the lesion responsible or the
episodes.
•$pecifc management or underl!ing causes.
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• The goal o the patients ph!sical eamination isto e&aluate or shock and blood loss.
• signs o shock include cool etremities, oliguria,chest pain, pre-s!ncope, conusion, and delirium.
• *ematemesis and melena should be noted.
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• $igns o chronic li&er disease should be noted,including
• spider angiomata,
• g!necomastia,
• splenomegal!,• ascites,
• pedal edema
• $igns o tumor are uncommon but indicate a poor
prognosis. $igns include a nodular li&er,abdominal mass, and enlarged and frm l!mphnodes.
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• )lood grouping and *htyping and cross !atching+
• Upper gastrointestinalendoscopy ,• In case o massi&e bleeding
ndoscop! should be carried out b!an eperienced operator as soonas the patient is resuscitated.
• /or patient %ith mild bleeding,endoscop! should be carried out onthe net morning ater admission.
• ccult )lood 'est,• +ormall! 0.1 blood is lost per da!.
• lood loss bet%een 12-322 ml (da!%ill produce melaena.
•
4T detects amount bet%een 32-12 m5(d.
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• &peci.c treat!ent"
• 'eptic Ulcers"
» ndoscopic hemostastasis
»
6edical management b! *0antagonist or 'I'
» $urgical treatment
• sophageal &arices"
» ndoscopic control b! electro-coagulation or in7ection
» 6edical treatment or 'ortalh!pertension..
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• &peci.c treat!ent"
• Gastric erosions"
» ndoscopic hemostastasis
» 6edical management b! *0 antagonist or
'I'
» $urgical treatment
• 6allor!-8eiss Tear"
» ndoscopic treatment
» I ails, gastrostom! and repair o the tear.
• 6alignanc!"» $hould be treated appropriatel!
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•ndoscopichemostastasis
•6edicalmanagement b!*0 antagonist or'I'
•$urgicaltreatment
•ndoscopiccontrol b! electro-coagulation or
in7ection•6edical treatmentor 'ortalh!pertension.
•ndoscopictreatment•I ails,
gastrostom! and repairo the tear.
$hould betreatedappropriatel!
•ndoscopichemostastasis
•6edicalmanagementb! *0antagonist or'I'
•$urgicaltreatment
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Terima *asih
elamat "ela&ar