MASTER CLASS

I L M U P E N YA K I T D A L A M
GASTROENTEROLOGY
d r. R e s t h i e R a c h m a n t a P u t r i
d r. M a r c e l a Yo l i n a

OFFICE ADDRESS:

Jakarta Medan
Jl. Layur Kompleks Perhubungan VIII No.52 RT.001/007 Jl. Setiabudi Kompleks Setiabudi Square No. 15
Kel. Jati, Pulogadung, Jakarta Timur Kel. Tanjung Sari, Kec. Medan Selayang 20132
WA. 081380385694/081314412212 WA/Line 082122727364

www.optimaprep.co.id
DISPEPSIA
 Dispepsia
• Dispepsia merupakan rasa tidak nyaman yang berasal dari daerah
abdomen bagian atas.

• Rasa tidak nyaman tersebut dapat berupa salah satu atau beberapa gejala
berikut yaitu:
– nyeri epigastrium,
– rasa terbakar di epigastrium,
– rasa penuh setelah makan, cepat kenyang, rasa kembung pada saluran cerna
atas, mual, muntah, dan sendawa.

• Dispepsia yang telah diinvestigasi terdiri dari dispepsia organik &

fungsional.
– Dispepsia organik terdiri dari ulkus gaster, ulkus duodenum, gastritis erosi,
gastritis, duodenitis dan proses keganasan
– Untuk dispepsia fungsional, keluhan berlangsung setidaknya selama tiga bulan
terakhir dengan awitan gejala enam bulan sebelum diagnosis ditegakkan.

Konsensus Nasional Penatalaksanaan Dispepsia dan Infeksi Helicobacter pylori. 2014.

 KLASIFIKASI DISPEPSIA FUNGSIONAL (ROMA III)
Epigastric pain syndrome
• Dispepsia fungsional dengan gejala
predominan nyeri epigastrium
• Diagnostic criteria* Must include all
of the following:
– Pain or burning localized to the
epigastrium of at least moderate
severity, at least once per week
– The pain is intermittent
– Not generalized or localized to other
abdominal or chest regions
– Not relieved by defecation or passage
of flatus
– Not fulfilling criteria for gallbladder
and sphincter of Oddi disorders
* Criteria fulfilled for the last 3 months
with symptom onset at least 6 months
prior to diagnosis
Post prandial distress
syndrome
• Dispepsia fungsional dengan gejala
predominan gejala ketidaknyaman
pada perut
• Diagnostic criteria (Must include one
or both of the following):
– Bothersome postprandial fullness,
occurring after ordinary-sized meals, at
least several times per week
– Early satiation that prevents finishing a
regular meal, at least several times per
week
* Criteria fulfilled for the last 3 months with
symptom onset at least 6 months prior to
diagnosis
• Supportive criteria
– Upper abdominal bloating or
postprandial nausea or excessive
belching can be present
– Epigastric pain syndrome may coexist
Ya Tidak
 Dispepsia
• Gejala predominan
– Nyeri epigastrium
 PPI
(omeprazole,
lansoprazole, dll)
– Cepat kenyang,
mual, muntah 
Agen prokinetik
(contoh:
metoklopramid,
domperidon)
• Dapat
dikombinasikan
antara PPI dan agen
prokinetik
GERD
 GERD
• Definition:
– Suatu gangguan di mana isi lambung mengalami
refluks secara berulang ke dalam esofagus, yang
menyebabkan terjadinya gejala dan/atau komplikasi
yang mengganggu.

• Symptoms:
– Heartburn; midline retrosternal burning sensation
that radiates to the throat, occasionally to the
intrascapular region.
– Others: regurgitation, dysphagia, regurgitation of
excessive saliva.

GI-Liver secrets
GERD
 Clinical Presentation of GERD
Typikal Ektraesofageal
• Heartburn
• Laryngitis
• Regurgitation
• Asthma

Atypikal • Sinusitis
• Chronic cough
• Chest pain
• Aspiration pneumonia
• Nausea
• Dental erosion
• Vomiting
• Bronchospasm
• Bloating
• Sore throat
• Dyspepsia
• Epigastric pain

Badillo R, et al. World J Gastrointest Pharmacol Ther. 2014.

Richter JE. Gastroenterol Clin North Am. 2007.
Alarm symptoms
• Progressive dysphagia
• Odynophagia
• Unknown weight loss
• New onset anemia
• Hematemesis and/or melena
• Familiy history with
malignancy of stomach
and/or esophagus.
• Persistent vomiting
 GERD-Q
Frekuensi skor untuk
No. Pertanyaan
gejala
0 2-3 4-7
1 hari
hari hari hari
Seberapa sering Anda mengalami perasaan terbakar di bagian belakang
1. 0 1 2 3
tulang dada Anda (heartburn)
Seberapa sering Anda mengalami naiknya isi lambung ke arah
2. 0 1 2 3
tenggorokan/mulut Anda (regurgitasi)
Seberapa sering Anda mengalami nyeri ulu hati?
3. 3 2 1 0

Seberapa sering Anda mengalami mual?

4. 3 2 1 0

Seberapa sering Anda mengalami kesulitan tidur malam oleh karena rasa
5. 0 1 2 3
terbakar di dada (hearburn) dan/atau naiknya isi perut?
Seberapa sering Anda meminum obat tambahan untuk rasa terbakar di
6. dada (heartburn) dan/atau naiknya isi perut (regurgitasi), selain yang 0 1 2 3
diberikan oleh dokter Anda? (seperti obat maag yang dijual bebas)

• Poin GerdQ < 7  GERD may be unlikely

• Poin GerdQ 8-18  probably GERD

Konsensus Nasional Penatalaksanaan GERD di Indonesia. 2013

 GERD Classification
• Non-erosive reflux disease/NERD
– 60-70% of GERD
– Normal endoscopy

• Erosive esophagitis
– 20-30% of GERD
– Endoscopy found mucosal break in esophagus
 Indication for Endoscopy
• Endoscopy in GERD indicated for patients:
– Had alarm symptoms
– The patient does not respond to the PPI empirical
therapy with a dose of 2 times a day.

• Endoscopy in GERD
– The findings of reflux esophagitis has specificity of 90-
95% for GERD.
– Los Angeles or Savary-Miller classification for severity
of esophagitis.

ASGE. Gastrointest Endosc. 2007

Konsensus Nasional Penatalaksanaan GERD di Indonesia. 2013
 Los Angeles Classification GERD

LA Grade A LA Grade B
Mucosal break <5 mm Mucosal break >5 mm

LA Grade D
LA Grade C
Mucosal break > 75% esophageal circumference
Mucosal break continuous between the tops of two or more
mucosal folds, <75% circumference
Sami SS, et al. Video J Encycloped GI Endosc. 2013
 GERD Complication: Barret’s Esophagus
(healthy esophageal epithelium is replaced with metaplastic columnar cells)
GERD Complication:Esophageal Cancer

Barium Swallow Endoscopy

 Tata laksana
 Non farmako: hindari pencetus, turunkan BB, hindari makan besar &
terlambat terutama 2-3 jam sebelum tidur, elevasi kepala saat tidur
 Farmako: PPI (sd 2x/hr), antacids, PPI menghilangkan 80–90% gejala;
ES: diare, ↑ risiko C. diff
 Bedah: fundoplication jika refrakter thhdp farmakologi: berhasil >
90%, tapi > 1⁄2 kembali ke farmakologi setelah 10 tahun
 Komplikasi
 Barrett’s esophagus: 10–15%
 Adenocarcinoma Esophageal: risiko 0.5%/tahun
 Tujuan Pengobatan
 Hilangkan gejala
 Sembuhkan esofagitis
 Tanggulangi dan cegah komplikasi
 Pertahankan remisi
GERD
ULKUS PEPTIKUM
 Characteristics
Duodenal Ulcer of DU and
Gastric UlcerGU
• May present < age 40 • Usually seen in
• Rarely associated with 50-60 year olds
NSAID use • Strong relationship to
• Pain often on empty NSAID use
stomach, better with food • Pain usually worse after
or antacids meals
• H. pylori in 90% to 100% • H. pylori in 70% to 90%

Both
• most common symptom: diffuse epigastric pain
• may be pain free
• may be associated with dyspeptic symptoms
• can lead to bleeding, perforation, or obstruction
 TATALAKSANA
• Medikamentosa:
ANTACID H2R Antagonis PPI SITOPROTEKTIF

• Memperingan • Antagonis • Inhibisi • Sukralfat:

gejala nyeri ulu reseptor H2, H+/K+ATPase. sebagai
hati/dyspepsia. sehingga • Bekerja amat protektan
• Paling umum menurunkan poten dalam • Membentuk
digunakan : sekresi asam menghambat lapisan
gabungan lambung. asam lambung pelindung yang
Al(OH)3 dan • Contoh: • Onset dalam 26 melapisi
Mg(OH)2 cimetidine, jam dengan mukosa
• Bekerja dengan ranitidine, durasi aksi 72- • Meningkatkan
menetralisir famotidine, 96 jam. proliferasi serta
asam lambung nizatidine. • Contoh obat: meningkatkan
berlebihan omeprazole, sintesis
lansoprazole, prostaglandin.
esomeprazole,
pantoprazole.
Sumber: Fauci, A.S. et al (2012) Harrison Principles of Internal Medicine. 18th Ed
Terapi Dietetik:
• Perubahan pola makan, menjauhi
makanan yang memicu gejala
dyspepsia harus dilakukan, antar
lain:
– Menghindari makanan pedas
– Menghindari kopi, karena kopi
dapat menyebabkan peningkatan
sekresi asam lambung serta
dihubungkan denganresiko infeksi
H. pylori
– Menghindari konsumsi alkohol
– Diet tinggi serat
• Pola makan teratur dengan
selingan makanan
Terapi Pembedahan:
Tatalaksana bedah dilakukan dengan
indikasi:
• Penyakit yang tidak respon
dengan pengobatan
medikamentosa
• Bedah cito bila terdapat
perforasi, karena meningkatkan
resiko peritonitis dan sepsis.
Bedah elektif:
• Vagotomy dan drainase
(pyloroplasty,
gastroduodenotomy,
gastrojejunotomy)
• Highly selective vagotomy
• Vagotomy dengan antrectomy
 Infeksi H. pylori
• Batang gram negative, berflagel, urease dan
katalase (+), mikroaerofilik
Helicobacter pylori memiliki faktor virulensi antara lain:

• Urease dapat menciptakan ammonia dari urea, mengakibatkan

UREASE peningkatan pH sehingga mendukung keidupan bakteri.

• untuk penempelan dengan mukosa lambung serta penarikan neutrophil

PicB dan serta monosit yang berperan dalam kerusakan mukosa lambung
ADHESIN

• berfungsi mendegradasi mucus serta lapisan pelindung mukosa.

PROTEASE
Infeksi H. pylori
Terapi Eradikasi H. pylori
GI BLEEDING
 GI Bleeding
• Bleeding from the gastrointestinal (GI) tract may present in 5 ways:
– Hematemesis: vomitus of red blood or "coffee-grounds" material.
– Melena: buang air besar berwarna hitam ter yang berasal dari saluran
cerna bagian atas. Yang dimaksud dengan saluran cerna bagian atas
adalah saluran cerna di atas (proksimal) ligamentum Treitz, mulai dari
jejunum proksimal, duodenum, gaster dan esophagus.
– Hematochezia: the passage of bright red or maroon blood from the
rectum.
– Occult GI bleeding: may be identified in the absence of overt bleeding
by a fecal occult blood test or the presence of iron deficiency.
– Present only with symptoms of blood loss or anemia such as
lightheadedness, syncope, angina, or dyspnea.

Harrison’s principles of internal medicine

 GI Bleeding
• Specific causes of upper GI bleeding may be suggested
by the patient's symptoms:
– Gastritis/gastropathy/duodenitis/Peptic ulcer:
• epigastric or right upper quadrant pain
– Esophageal ucer:
• odynophagia, gastroesophageal reflux, dysphagia
– Mallory-Weiss tear:
• emesis, retching, or coughing prior to hematemesis
– Variceal hemorrhage or portal hypertensive gastropathy:
• jaundice, weakness, fatigue, anorexia, abdominal distention
– Malignancy:
• dysphagia, early satiety, involuntary weight loss, cachexia
– Lesi Vascular
– Perdarahan Oropharyngeal & epistaxis  darah tertelan
Sumber: Simadibrata M, Rani AA. 11th Asian Pasific Congress of Gastroenterology and The 8th Asian Pasific Congress of
Digestive Endoscopy. Hongkong, March 10-14, 2000: B64 (A212).
Sumber: Laine L. Gastrointestinal bleeding. In: Kasper DL, Braumwald E, Fauci AS, editors. Harrison’s
Principles of Internal Medicine. 17th Edition. USA: McGraw Hill; 2008.p.257-60.
Penanganan pasien
STATUS HEMODINAMIK
 Tata laksana Umum
• Tirah baring, puasa, diet hati/lambung, pasang NGT
untuk dekompresi, pantau perdarahan
• Transfusi darah PRC (sesuai perdarahan yang terjadi
dan hb). Pada kasus varises transfusi sampai dengan hb
>10.
– Sementara menunggu darah dapat diberikan pengganti
plasma (misalnya dekstran/hemacel) atau nacl 0,9% atau rl
• Prosedur bedah dilakukan sebagai tindakan emergensi
atau elektif. Bedah emergensi di indikasikan bila pasien
masuk dalam keadaan gawat
Tatalaksana Khusus Perdarahan Variseal
• Tatalaksana perdarahan variseal
– Tamponade balon dalam 24 jam
– Obat vasoaktif
• Vasopresin 0,5-1mg/menit selama 20-60 menit
• Somatostatin 250 mcg bolus diikuti drip 250 mcg/jam
• Ocreotide drip 50 mcg/jam
– Endoskopi
– Profilaksis antibiotik
– Propanolol, dimulai dosis 2 x 10 mg dosis dapat ditingkatkan sampi tekanan
diastolik turun 20 mmHg atau denyut nadi turun 20% (setelah keadaan stabil
 hematemesis melena (-)
– Isosorbid dinitrat/mononitrat 2 x 1 tablet/hari setelah KU stabil
– Metoklorpramid 3 x 10 mg/hari
– Bila ada gangguan hemostasis obati sesuai kelainan
– Pada pasien dengan pecah varises/penyakit hati kronik/sirosis hati diberikan :
• Laktulosa 4 x 1 sendok makan
• Neomisin 4 x 500 mg/ Ciprofloxacin 2 x 500mg
• Obat ini diberikan sampai tinja normal.
Tatalaksana Khusus perdarahan non-
variseal (ulkus peptik)
– Endoskopi
• Perdarahan aktif  terapi endoskopik dan PPI IV
• Bekuan adheren  pertimbangkan terapi endoskopi dan PPI
IV
• Dasar bersih  tanpa terapi endoskopik dan PPI oral
– PPI IV  bolus 80 mg dilanjutkan drip 8 mg/jam
selama 72 jam.
– Untuk penyebab non varices :
• Injeksi antagonis reseptor H2 atau penghambat pompa
proton
• Sitoprotektor : Sukralfat 3-4 x 1 gram atau Teprenon 3 x 1 tab
• Injeksi vitamin K untuk pasien dengan penyakit hati kronis
atau sirosis hati
 Perdarahan Saluran Cerna Bawah (Hematoskezia)
• Definisi
– Hematoskezia = BAB darah segar berwarna merah yang berasal dari
saluran cerna bagian bawah
• Klinis
– diarrhea, tenesmus, hematochezia
– penyebab
• perdarahan diverticular (33%): 60% di colon dextra
• Neoplastic (19%): tes perdarahan samar
• Colitis (18%): infeksi, ischemic, radiasi, inflammatory bowel disease
• Angiodysplasia (8%): sering di colon ascending & cecum
• Anorectal (4%): hemorrhoids, fissura anal, ulkus rectal
• Lain2: post-polypectomy, vasculitis
• Tata laksana
– Non farmakologis: puasa, perbaikan hemodinamik. Jika hemodinamik
stabil dapat nutrisi enteral
– Farmakologis: Transfusi darah PRC/WB sampai dengan Hb > 10 gr%,
Infus cairan.Pengobatan infeksi sesuai penyebab. Bila ada kelainan
hemostasis di obati sesuai penyebabnya
DIARE
 Diare Akut
Definisi
• Diare berlangsung kurang dari 15 hari sejak awal
diare (menurut jurnal gastro 2004 < 4 minggu)

Tata laksana
• Atasi dehidrasi
• Antibiotic empirik untuk diare inflamasi: Shigella,
cholera, C. diff, Giardia, amebiasis, Salmonella
 Rehidrasi Cairan Pada Dewasa
Examination Mild hypovolemia Moderate hypovolemia Severe hypovolemia
Look at:
Mental status Alert Restless, irritable Lethargic or unconscious
Eyes Normal Sunken Very sunken and dry
Tears Present Absent Absent
Mouth/tongue Moist, slightly dry Dry Very dry
Drinks poorly or not able to
Thirst Increased thirst Thirsty, drinks eagerly
drink
Feel:
Goes back very slowly
Skin pinch Goes back rapidly Goes back slowly
(tenting)
Very fast, weak or
Pulse Normal Rapid, weak
nonpalpable
From 5 to 10 percent of
Extent of volume loss <5 percent of body weight >10 percent of body weight
body weight
Estimated fluid deficit <50 mL/kg 50-100 mL/kg >100 mL/kg

Adapted from: Swerdlow DL, Ries AA. JAMA 1992; 267:1495 and World Health Organization. The treatment of diarrhea: A manual
for physicians and other senior health workers, 4th revision. WHO/FCH/CAH/05.1. World Health Organization, Geneva 2005.
(Available at http://whqlibdoc.who.int/publications/2005/9241593180.pdf).
 PATHOGEN KLINIS
Non inflamasi Gangguan absorpsi & sekresi, diare dgn ampas, leukosit & eri (-)
Toksin Keracunan makanan < 24 jam S. aureus (daging & susu), B cereus (nasi
goring), C Perfringens (daging)
Viral Rotavirus Menular, penitipan anak, 4-8 hari
Norovirus 50 % semua diare daerah dingin, 1-3 hari, dominan muntah
Bakteri E coli (toxin) > 50% diare daerah berkembang, <7 hari
V cholera BAB cucian beras, dehidrasi & gang elektrolit berat
Parasit Giardia Lewat air, wabah, kembung
Cryptosporodia Lewat air, wabah, sembuh sendiri, nyeri perut 80%, demam 40%
Cyclospora Produk kontaminasi
Inflamasi Invasi kolon. Diare ampas sedikit, kram perut, tenesmus, demam, bisa
leukosit & eri (+)
Bakteri Campylobacter Unggas mentah, susu belum dipasteur, dibawa kucing/anjing, GBS

Salmonella (non typhoid) Telur, unggas, susu

Shigella Menular, perdarahan massif & pus di feses, leukosit (+)
E Coli (EHEC) Daging mentah, susu belum dipasteur, eritrosit (+)
Salmonella typhi Demam, bradikardi relative, lidah tifoid
Parasite E hystolytica Tenesmus, abses hepar
Virus CMV Pasien Immunosupresi
 Kolera
• Infeksi yang menyerang usus halus,
disebabkan oleh Vibrio cholerae. • Tatalaksana:
– Tatalaksana utama:
• Profuse watery diarrhea, muntah, dan REHIDRASI
kram perut. Sering menyebabkan
dehidrasi dan syok.
– Pemberian zinc
– Tatalaksana adjunctive:
• Penegakan diagnosis: antibiotik (antibiotik
– Kultur dengan media TCBS diberikan untuk
– Pemeriksaan feses dengan memperpendek masa sakit)
mikroskop lapang gelap
Class Antibiotic Typical pediatric dose* Adult dose
Doxycycline 4-6 mg/kg (single dose) 300 mg (single dose)
Tetracyclines 50 mg/kg/day in four equally divided doses, for 500 mg four times per day for
Tetracycline
three days three days

Azithromycin 20 mg/kg (single dose) 1 g (single dose)

Macrolides 40 mg/kg/day in four equally divided doses, for 500 mg four times per day for
Erythromycin
three days three days

Fluoroquinolones Ciprofloxacin 20 mg/kg (single dose) 1 g (single dose)

https://www.uptodate.com/contents/image?imageKey=ID%2F71548&topicKey=ID%2F2704&search=cholera&rank=1~85&source=see_link
 Diarrheagenic Escherichia coli

Strain Syndrome
Enterotoxigenic E. coli (ETEC) Watery diarrhea
Enteropathogenic E. coli (EPEC) Infantile diarrhea
Hemorrhagic colitis and hemolytic
Enterohemorrhagic E. coli (EHEC)
uremic syndrome
Enteroinvasive E. coli (EIEC) Dysentery
Persistent diarrhea in children and
Enteroaggregative E. coli (EAEC)
patients infected with HIV

https://www.uptodate.com/contents/image?topicKey=ID%2F2720&view=machineLearning&search=eiec&sectionRank=1&usage_type=default&imageKey=ID
%2F67152&rank=1~5&source=machineLearning&display_rank=1
 Diarrheagenic Escherichia coli
Noninflammatory Diarrheas
Enterotoxigenic E. coli (ETEC)
Inflammatory Diarrheas
Enteroinvasive E. coli (EIEC)
Enteropathogenic E. coli (EPEC)
Shigatoxin-producing E. coli
(STEC)/EHEC
Enteroaggregative E. coli (EAggEC)
Rapid onset of watery, nonbloody diarrhea of considerable
volume, accompanied by little or no fever. Diarrhea and
other symptoms cease spontaneously after 24 to 72 hours
Present most commonly as watery diarrhea. Minority of
patients experience a dysentery syndrome, with fever,
systemic toxicity, crampy abdominal pain, tenesmus, and
urgency
Profuse watery, nonbloody diarrhea with mucus, vomiting
and low-grade fever. Chronic diarrhea and malnutrition can
occur. Usually at < 2 y.o, esp <6 mo (at weaning period)
Symptoms ranging from mild diarrhea to severe
hemorrhagic colitis and hemolytic-uremic syndrome in all
ages
Watery, mucoid, secretory diarrhea with low-grade fever
and little or no vomiting. One third of patients have grossly
bloody stools. The watery diarrhea usually persist ≥14 days
 Disentri: Basiler vs Amoeba
Characteristics Amoebic dysentery Bacillary dysentery
Macroscopic
Number 6-8 motions a day Over 10 motions a day
Blood mucus, mainly watery
Appearance and Amount Blood mucus, semi formed
Odour Offensive (fishy odour) Odourless
Colour Dark red (altered blood) Bright red (fresh blood)
Reaction Acidic Alkaline
Consistency Not adherent to the container Adherent to the container
Microscopic
Discrete, sometimes in clumps due to
RBCs In clumps
rouleaux formation
Pus Cells Few Numerous
Numerous, many of them contain
Macrophages Few RBCs hence may be mistaken for E.
histolytica
Eosinophils Present Scarce
Charcot-Leyden (C-L) crystals* Present Absent
Pyknotic bodies** Present Absent
Ghost Cells*** Absent Present
Parasites Seen Trophozoites of E. histolytica Absent
Scanty, nonmotile (Shigella is non
Bacteria Seen Many motile bacteria
motile bacteria)
Culture
Pure growth of Shigella spp. may be
Growth on MacConkey Agar Various intestinal flora may grow
seen
 Amoebiasis ec E. Histolitica

AMOEBIASIS AMOEBIASIS
INTESTINAL EKSTRAINTESTINAL
• Masa inkubasi: 8 hari hingga • Abses liver
beberapa bulan
• Kolitis amuba: nyeri perut • Penyakit pleuropulmonal
kuadran bawah, distensi
• Peritonitis
• Tahap Akut • Perikarditis
– Diare dengan epitelium (tanpa
darah, nyeri perut, << BB, flatulens • Abses otak
dan konstipasi
• Penyakit genitourinaria
• Infeksi Berat
– 10-20 hari
– Diare dengan epitelium dan darah,
nyeri perut (mulas), dehidrasi dan
demam
 Amoebiasis
ALUR INFEKSI

• Kista infektif (kista

matang, berinti 4)
tertelan  Ekskistasi di
ileum terminal/ kolon
 trofozoit (bentuk
invasif)  penetrasi
dan invasi ke mukosa
kolon  destruksi
jaringan, diare
berdarah, dan kolitis

• Trofozoit juga bisa

menyebar secara
hematogen lewat
sirkulasi portal ke hati
atau organ jauh
http://emedicine.medscape.com/article/212029-overview
 Siklus Hidup E. Histolitica

Division of
Excystatiton in
Ingestion of quadrinucleate cyst
small
cysts into 4 and then 8
intestine
trophozoites

Trophozoites
Excretion of
Encystation move to
cysts
colonize colon

Ingestion of
cysts by the
patient
 Amoebiasis: Diagnosis
• Laboratorium
– Leukositosis tanpa eosinofilia (80%)
– Peningkatan alkaline phosphatase (80%)
– Peningkatan kadar transaminase dan bilirubin
– Penurunan albumin dan anemia

• Mikroskopik  terlampir

• Feses: adanya bentuk tropozoit dan kista

• Pewarnaan Lugol pada jaringan terinfeksi

• USG
– Abses hati amoeba: lesi bulat hipoekoik homogen soliter di
aspek posterior lobus kanan hati (70-80%)
http://emedicine.medscape.com/article/212029-workup#c7
 Amoebiasis: Gambaran Mikroskopik

Trofozoit dari
Entamoeba histolytica

Kista Imatur Entamoeba histolytica

(kista matur memiliki 4 nuklei)

Sel darah
Central
merah
Karyosome
 Amoebiasis: Tatalaksana
• Metronidazol
– 3 x 500-750 mg/hari selama
5-10 hari
– Abses hati: 3 x 750 mg/hari
selama 10 hari
• Tinidazole
– Intestinal amebiasis 1 x 2 g
selama 3 hari
– Amebic liver abscess 1 x 2 g
selama 3-5 hari
Amoebiasis vs Infeksi Pencernaan Lain
P E N YA K I T ETIOLOGI GEJALA KLINIS T E L U R / K I S TA
Psedoupodium
Entamoeba
AMOEBIASIS Diare berdarah, nyeri perut, tenesmus dengan sel darah
histolytica
didalamnya
Anemia (hidup di sekum- colon Tempayan dengan
Tricuris
TRICURIASIS asendens) gejala diare-disentri atau penonjolan pada
trichuria
tanpa gejala kedua kutubnya
Berdinding tebal,
Balantidium
BALANTIDIASIS Sindroma disentri bervakuola,
coli
makronukleus
Telur dibungkus
T. Solium/ T. Nyeri ulu hati, mual, muntah,
TAENIASIS embriofor yang
Saginata mencret, obstipasi dan pusing
bergaris radial

Aktif: berflagel, In
Giardia aktif: oval, dinding
GIARDIASIS Diarrhea, Malodorous, greasy stools
intestinalis tipis dan kuat, berinti
2-4
E. Histolytica Taenia S. B. Coli

Trichuris Trichuria Giardia Lamblia

 Disentri Basiler:
Etiologi, Gejala, Tatalaksana
Etiologi Gejala dan Tatalaksana

Shigella dysentriae Stool frequency is typically 8 to 10 per day, but may increase to up to 100 per day. Bloody
stools, abdominal cramps, and tenesmus, particularly if accompanied by fever. Nausea
and vomiting are notably absent in most patients.
DOC: Ciprofloxacin/ Levofloxacin, Azitromisin, Cefixime, Ceftriaxone.

EIEC Symptoms are similar with Shigellosis. Treatment: Rehydration.

EHEC Bloody diarrhea, no reported fever, abdominal tenderness. Hemolytic-uremic syndrome is

a major complication of EHEC infection. Antibiotic therapy is generally not beneficial in
patients with EHEC infection.

Campylobacter jejuni Characterized by cramping, periumbilical abdominal pain, and diarrhea. The pain may
become continuous and radiate to the right iliac fossa, mimicking acute appendicitis.
Nausea is common. Antibiotics are not needed for most cases of C. jejuni gastroenteritis.
First line agents for treatment of Campylobacter gastroenteritis include fluoroquinolones
or azithromycin.

Salmonella The diarrhea is typically not grossly bloody, although bloody stools can be seen,
particularly among children. The cardinal features include diarrhea, nausea, vomiting,
fever, and abdominal cramping. Fluoroquinolones (eg, ciprofloxacin 500 mg orally twice
daily or levofloxacin 500 mg orally once daily) are generally the most appropriate agents
for adults and adolescents without contraindications to these medications.
KERACUNAN MAKANAN
(FOOD POISONING)
 Source and Diagnosis and
Causative Agents Symptoms
Clinical Features Treatment
Improperly stored foods Intense vomiting and
with high salt or sugar watery diarrhea start 1-4 h
Staphylococci Symptomatic treatment
content favors growth of after ingestion and last as
staphylococci. long as 24-48 h
Vomiting and cramps.
Mainly vomiting after 1-6
h and mainly diarrhea
B cereus Contaminated fried rice Symptomatic treatment
after 8-16 h after
ingestion; lasts as long as
1d
Acute onset of abdominal
cramps with diarrhea
Culture of clostridia in
Inadequately cooked starts 8-24 h after
C perfringens food and stool
meat, poultry, or legumes. ingestion.
Symptomatic treatment
Vomiting is rare. It lasts
less than 1 d.
Descending weakness and Toxin present in food,
Canned foods (eg, smoked paralysis start 1-4 d after serum, and stool.
C botulinum fish, mushrooms, ingestion, followed by Respiratory support
vegetables, honey) constipation. Mortality is Intravenous trivalent
high. antitoxin from CDC
 Raw and pasteurized milk, soft Systemic disease associated
CSF or blood culture
cheeses, raw vegetables, with bacteremia; Intestinal
Listeria monocytogenes Must treat with antibiotics if
shrimp. symptoms precede systemic
bacteremic
disease.
Acute-onset watery diarrhea
starts 24-48 h after ingestion
Enterotoxic E coli(eg, Contaminated water and food Supportive treatment
Concomitant vomiting and
traveler's diarrhea) (eg, salad, cheese, meat) No antibiotics
abdominal cramps may be
present. It lasts for 1-2 d.
Usually progresses from
watery to bloody diarrhea. It
lasts for 3-8 d; May be Diagnosis with stool culture
Enterohemorrhagic E Improperly cooked hamburger
complicated by hemolytic- Supportive treatment
coli (eg, E coliO157:H7) meat and previously spinach.
uremic syndrome or No antibiotics
thrombotic thrombocytopenic
purpura
Contaminated imported Usually watery diarrhea (some Supportive treatment
Enteroinvasive E coli
cheese. may present with dysentery). No antibiotics
Implicated in traveler's Ciprofloxacin may shorten
Enteroaggregative E coli diarrhea in developing Can cause bloody diarrhea duration and eradicate the
countries organism
Prompt replacement of fluids
and electrolytes (oral
Large amount of nonbloody
rehydration solution)
V cholera Contaminated water and food. diarrhea starts 8-24 h after
Tetracycline (or
ingestion. It lasts for 3-5 d.
fluoroquinolones) shortens the
duration of symptoms
DEFISIENSI VITAMIN
 Defisiensi Vitamin B
Jenis Vitamin Gejala
Beriberi - a disease whose symptoms include weight loss,
Vitamin B1 (Thiamine) body weakness and pain, brain damage, irregular heart rate,
heart failure, and death if left untreated
Causes distinctive bright pink tongues, although other
Vitamin B2 (Riboflavin) symptoms are cracked lips, throat swelling, bloodshot eyes,
and low red blood cell count
Pellagra - symptoms included diarrhea, dermatitis, dementia,
Vitamin B3 (Niacin)
and finally death (4D)
Vitamin B5
Acne and Chronic paresthesia
(Pantothenic Acid)
Microcytic anemia, depression, dermatitis, high blood
Vitamin B6
pressure (hypertension), water retention, and elevated levels
(Pyridoxine)
of homocysteine
Causes rashes, hair loss, anaemia, and mental conditions
Vitamin B7 (Biotin)
including hallucinations, drowsiness, and depression
Causes gradual deterioration of the spinal cord and very
Vitamin B12
gradual brain deterioration, resulting in sensory or motor
(Cobalamin)
deficiencies
 Defisiensi Vitamin C/ Asam Askorbat
• Menyebabkan penyakit scurvy • Vitamin C diabsorbsi lewat
• Gejala + Tanda pencernaan  defisiensi
– Memar pada kulit disebabkan kurangnya asupan
– muscle fatigue vit C dalam makanan/
meningkatnya kebutuhan
– Gusi bengkak dan mudah
berdarah (traumya/ adanya stressor
– Luka sulit sembuh
yang berat)
– Purpura • Dosis treatment:
– Osteopenia – 100-300mg/hari PO/IM/IV/SC
dibagi dua dosis
– Anemia
– Malaise
– Letargi
– Neuropati
– Perifollicular hyperkeratotic
papules
Defisiensi Vitamin Lainnya
IBS
 IBS
• Irritable Bowel Syndrome (IBS)
– kelainan fungsional usus kronik berulang dengan
nyeri atau rasa tidak nyaman pada abdomen yang
berkaitan dengan defekasi atau perubahan
kebiasaan buang air besar setidaknya selama 3
bulan.
• Rasa kembung, distensi, dan gangguan
defekasi merupakan ciri-ciri umum dari IBS.
• Tidak ada bukti kelainan organik.
Konsensus IBS. Perhimpunan Gastroenterologi Indonesia. 2013
 IBS
Menurut kriteria Roma III, IBS dibagi menjadi 3 subkelas yaitu:
– IBS dengan diare (IBD-D):
• Feses lembek/cair ≥25% waktu dan feses padat/bergumpal <25% waktu
• Ditemukan pada sepertiga kasus
• Lebih umum ditemui pada laki-laki
– IBS dengan konstipasi (IBS-C):
• Feses padat/bergumpal ≥25% waktu dan feses lembek/cair <25% waktu
• Ditemukan pada sepertiga kasus
• Lebih umum ditemui pada wanita
– IBS dengan campuran kebiasaan buang air besar atau pola
siklik (IBS-M)
• Feses padat/bergumpal dan lembek/cair ≥25% waktu
• Ditemukan pada sepertiga kasus
– Catatan : yang dimaksud dengan 25% waktu adalah 3 minggu
dalam 3 bulan.
Konsensus IBS. Perhimpunan Gastroenterologi Indonesia. 2013
 IBS
Kriteria diagnostik
• Nyeri abdomen atau rasa tidak nyaman berulang
selama 3 hari dalam sebulan pada 3 bulan
terakhir dengan 2 atau lebih gejala berikut
– Perbaikan dengan defekasi
– Onset terkait dengan perubahan frekuensi BAB
– Onset terkait dengan perubahan bentuk dan tampilan
feses
• Kriteria diagnostik terpenuhi selama 3 bulan
terakhir dengan onset gejala setidaknya 6 bulan.

Konsensus IBS. Perhimpunan Gastroenterologi Indonesia. 2013

 Tatalaksana IBS
• Non farmakologi
– IBS tipe konstipasi
• diet tinggi serat
– IBS tipe diare
• membatasi makanan yang mencetuskan gejala
• Farmakologi
– IBS-C
• bulking agent, laksatif, antagonis reseptor 5HT3 (prucalopride),
aktivator kanal klorida C2 selektif (lubiprostone)
– IBS-D
• antidiare (loperamide), antagonis reseptor 5HT3, antidepresan
– Nyeri, kembung dan distensi
• antispasmodik, antibiotik (rifaximin), probiotik, antidepresan

Konsensus IBS. Perhimpunan Gastroenterologi Indonesia. 2013

INFLAMMATORY BOWEL DISEASE
 IBD
• IBD: penyakit kronik karena aktiviasi
imun di mukosa saluran cerna.

• Kolitis ulseratif
– Gejala utama kolitis ulseratif adalah
diare dengan/tanpa darah.
– Gejala lainnya meliputi tenesmus,
urgency, nyeri rektal, pasase mukus
tanpa diare.
– Nyeri tekan biasanya terdapat di kiri
bawah.
– Lokasi lesi bervariasi dari
proctosigmoiditis, lef-sided disease
sampe proksimal kolon desenden,
hingga universal colitis.

• Crohn disease
– Lesi bisa di area saluran cerna manapun.
– Gejala diare, nyeri abdomen biasanya di
kanan bawah, memberat setelah makan,
– Nyeri tekan, massa akibat inflamasi di
kanan bawah

Robbins & Kumar Pathologic basis of disease. 2010.

Difference Crohn’s Disease Ulcerative Colitis
Most common site Terminal ileum Rectum
Distribution Mouth to anus Rectum to colon “backwash” ileitis
Spread Discontinuity “skip” lesions Continuous
Endoscopy •Focal aphthous ulcers with intervening •Extensive ulceration
normal mucosa •Pseudo-polyps
•Linear fissures
•Cobblestone appearance
•Thickened bowel wall “linitis plastic”
•Creeping fat
Pathology Noncaseating granulomas Crypt abscess
Inflammation Transmural Limited to mucosa and submucosa

Complication •Strictures •Toxic megacolon

•String sign on barium study
•Obstruction
•Abscess
•Fistula
•Sinus tract
Genetic Association HLA-B27
Extraintestinal Uncommon Common
manifestation
Cancer risk Slight 1-3% 5-25%
Presentation Variable : Pain, diarrhea, weight loss Bloody diarrhea
Perbedaan Histopatologi IBD
 IBD
Histopatologi Endoskopi
PANKREATITIS
 PANKREATITIS AKUT
DEFINISI
• Reaksi peradangan pankreas yang akut

KLINIS
• Dispepsia sedang sampai berat, gelisah kadang disertai gangguan kesadaran
• Demam, ikterus, gangguan hemodinamik, syok dan takikardia, bising usus menurun (
ileus paralitik)
• Pankreatitis akut berat dapat mengalami sesak napas karena inflamasi diafragma
akibat pankreatitis, efusi pleura, atau adult respiratory distress syndrome.
• Pemeriksaan fisik: Nyeri tekan abdomen, defans, tanda perdarahan retroperitoneal
(Cullens – periumbilical, Grey Turners – pinggang) jarang terlihat

PENEGAKAN DIAGNOSIS
• Amylase & lipase ↑
– Amilase meningkat pada 6-12 jam dari onset pankreatitis. Lipase meningkat pada 24 jam-14 hari
dari onset pankreatitis.
• MRI
• MRCP (bila terdapat dugaan bahwa pankreatitis disebabkan oleh koledokolithiasis)

https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-acute-pancreatitis
 A. Cullen Sign
B. Grey-Turner Sign
 Etiologi Pankreatitis Akut
Gallstones, biliary sludge, ascariasis, periampullary diverticulum, pancreatic or periampullary cancer,
Mechanical
ampullary stenosis, duodenal stricture or obstruction

Toxic Ethanol, methanol, scorpion venom, organophosphate poisoning

Metabolic Hyperlipidemia (types I, IV, V), hypercalcemia

Didanosine, pentamidine, metronidazole, stibogluconate, tetracycline furosemide, thiazides, sulphasalazine,

Drugs
5-ASA, L-asparaginase, azathioprine, valproic acid, sulindac, salicylates, calcium, estrogen

Viruses-mumps, coxsackie, hepatitis B, CMV, varicella-zoster, HSV, HIV

Infection Bacteria-mycoplasma, Legionella, Leptospira, salmonella

Fungi-aspergillus
Parasites-toxoplasma, cryptosporidium, Ascaris
Trauma Blunt or penetrating abdominal injury, iatrogenic injury during surgery or ERCP (sphincterotomy)
Congenital Cholodochocele type V, pancreas divisum*
Vascular Ischemia, atheroembolism, vasculitis (polyarteritis nodosa, SLE)
Miscellaneous Post ERCP, pregnancy, renal transplantation, alpha-1-antitrypsin deficiency
Genetic CFTR, PRSS1, SPINK1, and other genetic mutations

https://www.uptodate.com/contents/image?imageKey=GAST%2F78423&topicKey=GAST%2F5652&search=pancreatitis&rank=1~150&source=see_link
Klasifikasi Pankreatitis
 Tatalaksana
Pankreatitis
Akut

https://teachmemedicine.org/cleveland-clinic-acute-pancreatitis/
American College of Gastroenterology Guideline:
Management of Acute Pancreatitis, 2013
IKTERUS/JAUNDICE
 Ikterus

Fundamentals of urine & body fluid analysis. 3rd ed. 2013.

 Ikterus

Fundamentals of urine & body fluid analysis. 3rd ed. 2013.

Ikterus

Pathophysiology of disease
 Ikterus

Fundamentals of urine & body fluid analysis. 3rd ed. 2013.

Ikterus
 Ikterus

Cek Urobilin & Bilirubin

Urobilin – Urobilin + Urobilin ++

Bilirubin urin+ + Bilirubin urin + Bilirubin urin -
Bilirubin Direct > Bilirubin Direct + Bilirubin Direct N
Bilirubin Indirect + Bilirubin Indirect >

Parenkim
Obstruksi:
- Hepatitis Hemolitik
- Intra hepatic
-Cirrhosis
- Extra hepatic
-Hepatoma

USG:Bile duct dilatation CT scan

PTC Tumor
ERCP Batu
Intra hepatal : hepatitis Extra hepatal MRI

Flow chart pasien dengan ikterus

Ikterus
HEPATITIS
 Hepatitis
• Inflamasi hepar yang disebabkan oleh berbagai macam penyebab.
• Penyebab hepatitis: autoimun, hepatitis imbas obat, virus, alkohol,
dan lain-lain.
• Virus hepatitis merupakan infeksi sistemik yang dominan
menyerang hepar. Hepatitis jenis ini paling sering disebabkan oleh
virus hepatotropik (virus Hepatitis A, B, C, D, E).
• Incubation periods for hepatitis A range from 15–45 days (mean, 4
weeks), for hepatitis B and D from 30–180 days (mean, 8–12
weeks), for hepatitis C from 15–160 days (mean, 7 weeks), and for
hepatitis E from 14–60 days (mean, 5–6 weeks).
Harrison’s principles of internal medicine. 18th ed. 2011.
 Hepatitis A
• Hepatitis A IgM
antibodies are
usually detectable 3
to 4 weeks after an
initial exposure and
return to normal after
about 8 weeks.
• Hepatitis A IgG
antibodies may begin
to develop 2 weeks
after the IgM
antibodies increase to
a high level.
Hepatitis B clinical course
 HEPATITIS VIRUS
• HBsAg (the virus coat, s= surface)
– the earliest serological marker in the serum.
• HBeAg
– Degradation product of HBcAg.
– It is a marker for replicating HBV.
• HBcAg (c = core)
– found in the nuclei of the hepatocytes.
– not present in the serum in its free form.
• Anti-HBs
– Sufficiently high titres of antibodies ensure
imunity.
• Anti-Hbe
– suggests cessation of infectivity.
• Anti-HBc
– the earliest immunological response to HBV
– detectable even during serological gap.

Principle & practice of hepatology.

Hepatitis
Hepatitis C
 90% transfusion,
50% IDU
 Little evidence of
sexual or perinatal
transmission
 Incubation 1-5 (2)
mo
 Acute infection:
 75% subclinical
 25% jaundice
 Chronicity
 50%
 Cirrhosis: 20% of
chronic
HEPATOBILIER
PENYAKIT HEPATOBILIER
 Lokasi Nyeri Anamnesis Pemeriksaan Pemeriksaan Diagnosis Terapi
Fisis Penunjang
Urea breath test (+): H.
pylori
Membaik dgn makan PPI: ome/lansoprazol
Endoskopi:
Nyeri epigastrik (ulkus duodenum), H. pylori:
Tidak spesifik eritema (gastritis akut) Dispepsia
Kembung Memburuk dgn makan klaritromisin+amoksili
atropi (gastritis kronik)
(ulkus gastrikum) n+PPI
luka sd submukosa
(ulkus)

Nyeri tekan & defans,

Gejala: mual &
perdarahan
muntah, Demam Peningkatan enzim Resusitasi cairan
Nyeri epigastrik retroperitoneal
Penyebab: alkohol amylase & lipase di Pankreatitis Nutrisi enteral
menjalar ke punggung (Cullen: periumbilikal,
(30%), batu empedu darah Analgesik
Gray Turner:
(35%)
pinggang), Hipotensi

Prodromal (demam,
Nyeri kanan atas/ Transaminase, Serologi
malaise, mual)  Ikterus, Hepatomegali Hepatitis Akut Suportif
epigastrium HAV, HBSAg, Anti HBS
kuning.
Risk: Female, Fat,
Fourty, Hamil Nyeri tekan abdomen
Nyeri kanan atas/ USG: hiperekoik dgn Kolesistektomi
Prepitasi makanan Berlangsung 30-180 Kolelitiasis
epigastrium acoustic window Asam ursodeoksikolat
berlemak, Mual, TIDAK menit
Demam

Resusitasi cairan
Nyeri epigastrik/ USG: penebalan dinding
Mual/muntah, AB: sefalosporin gen.
kanan atas menjalar Murphy Sign kandung empedu Kolesistitis
Demam 3 + metronidazol
ke bahu/ punggung (double rims)
Kolesistektomi
Kolelitiasis
• Definisi
– Batu di kandung empedu
– Empedu – garam empedu, phospholipid,
kolesterol; ↑ saturasi kolseterol di empedu +
mempercepat nukleasi + hypomotilitas kandung
empedu batu empedu
• Klinis
– Tipe: batu kolesterol 90%, batu pigmen 10%
– Kolik bilier: nyeri perut kanan atas atau
epigastrium, tiba2, bertahan 30 menit sd 3 jam,
menjalar ke scapula, mual
– Dipicu makanan berlemak
• Tata laksana
– Cholecystectomy (CCY), laparoscopic, jika
symptomatik
– Ursodeoxycholic acid (jarang) untuk batu
cholesterol jika tidak bisa operasi
• Komplikasi
– Kolsesistitis
– Koledokolitiasis  kolangitis
 Koledokolitiasis
• Definisi
– Batu di duktus biliaris
koledokus
• Klinis
– Asymptomatic (50%)
– Kolik bilier: nyeri perut
kanan atas atau
epigastrium, tiba2,
bertahan 30 menit sd 3
jam, menjalar ke scapula,
mual
– Obstruksi bilier  ikterik,
pruritis, mual
• Tata laksana
– ERCP & papillotomy
– CCY
• Komplikasi
– Cholangitis, cholecystitis,
pancreatitis, stricture
 Cholecystitis
• Cholecystitis is inflammation of the gallbladder that occurs
most commonly because of an obstruction of the cystic duct
by gallstones arising from the gallbladder (cholelithiasis).
• Clinical symptoms of acute cholecystitis include abdominal
pain (right upper abdominal pain), nausea, vomiting, and
fever
• Jaundice may be noted in approximately 15% of patients
• Murphy’s sign are the characteristic findings of acute
cholecystitis.
• A positive Murphy’s sign has a specificity of 79%–96% for
acute cholecystitis.
 Penyakit Hepatobilier
• Diagnosis kolesistitis:
– Murphy sign atau nyeri tekan
abdomen kanan atas
– Demam, leukositosis, atau
peningkatan CRP
– USG: ditemukan batu (90-95%
kasus), tanda inflamasi kandung
empedu (penebalan
dinding/double rim cairan
perikolesistik, dilatasi duktus
biliaris)

• Temuan lab lainnya:

– aminotransferase meningkat
sedang (biasanya <5 kali batas atas)
– Bilirubin meningkat ringan (<5
mg/dL), bila tinggi kemungkinan
koledokolitiasis

Harrison’s principles of internal medicine. 19th ed. McGraw-Hill

Pocket medicine. 4th ed. Lippincott Williams & Wilkins.
Diagnostic criteria and severity assessment of acute cholecystitis: Tokyo Guidelines. J Hepatobiliary Pancreat Surg. 2007 Jan; 14(1): 78–82.
 Penyakit Hepatobilier
• Temuan USG kolesistitis:
– Sonographic Murphy sign
(nyeri tekan timbul ketika
probe USG ditekan ke arah
kandung empedu)
– Penebalan dinding kandung
empedu (>4 mm)
– Pembesaran kandung
empedu (long axis diameter
>8 cm, short axis diameter
>4 cm)
– Impacted stone,
pericholecystic fluid
collection
Diagnostic criteria and severity assessment of acute cholecystitis: Tokyo Guidelines. J Hepatobiliary Pancreat
Surg. 2007 Jan; 14(1): 78–82.
Murphy sign
 Penyakit Hepatobilier
Kolesistitis
• Terapi Medik
– Puasa, NGT, tatalaksana cairan & elektrolit
– NSAID untuk analgesik karena lebih sedikit menimbulkan
spasme sfingter Oddi daripada morfin.
– Antibiotik IV: piperacillin, ampicillin sulbactam,
ciprofloxacin, moxifloxacin, & sefalosporin generasi 3.
• Terapi Bedah
– Waktu optimal untuk operasi tergantung kestabilan pasien.
– Kolesistektomi dini (dalam 72 jam) merupakan terapi
pilihan pada sebagian besar pasien kolesistitis akut.
 Kolangitis
• Definisi
– Obstruction duktus koledokus biliar  infeksi
sisi proximal dari obstruksi

• Etiologi:
– Batu duktus bilier/ koledokolitiasia (85%)
– Keganasan (biliar, pancreas) atau striktur jinak
– Infiltrasi cacing (Clonorchis sinensis,
Opisthorchis viverrini)

• Klinis
– Charcot’s triad: nyeri perut kanan atas, ikterik,
demam/menggigil; 70%
– Reynold’s pentad: Charcot’s triad + shock dan
gangguan kesadaran;15%

• Tata laksana
– Antibiotik (broad spectrum) :ampicillin +
gentamicin (atau levofloxacin) + MNZ (jika
berat); carbapenems; pip/tazo
– 20% butuh dekompresi bilier cito via ERCP
(papillotomy, extraksi, stent).
SIROSIS HEPATIS
 Sirosis Hepatis
• Sirosis hepatis adalah stadium akhir fibrosis hepatik
progresif ditandai dengan distorsi arsitektur hepar dan
pembentukan nodul regeneratif.
• Terjadi akibat nekrosis hepatoseluler
– Sirosis hati kompensatabelum ada gejala klinis, namun
dapat ditemukan gejala awal mudah lelah, lemas, nafsu
makan berkurang, mual, BB turun
– Sirosis hati dekompensata gejala klinis yang jelas
(komplikasi gagal hati dan hipertensi porta)
• Etiologi:
- Alkohol, hepatitis, biliaris, gagal jantung, metabolik, obat
- Etiologi tersering di Indonesia: hepatitis B (40-50%)

Buku Ajar Ilmu Penyakit Dalam

Patofisiologi
STIGMATA SIROSIS
 Ensefalopati Hepatikum
• Kerusakan hepar 
metabolisme ammonia
menurun kadar
ammonia meningkat
Ensefalopati Hepatikum
 Ensefalopati Hepatikum
• Lactulose
– first-line therapy of HE  menurunkan pH kolon dan
mengganggu uptake glutamin pada mukosa usus 
menurunkan sintesis dan absorbsi amonia.
• Antibiotic (rifaximin, neomycin)
– menghambat glutaminase mukosa saluran cerna 
menurunkan produksi amonia di usus.
• Sodium benzoat
– berinteraksi dengan glisin membentuk hipurat,
senyawa yang membutuhkan amonia ketika diekskresi
di renal.
 Cirrhosis
• Therapy
– improve mental status by
diminishing the
absorption of ammonia &
other noxious substances
from the GI tract.

• Lactulose (nonabsorbable
carbohydrate) 
metabolized by microbes
 acidic environment 
trap ammonia as charged
NH4+  excreted by the
resultant osmotic diarrhea.

Pathophysiology of disease. 2nd ed. Springer; 2006.

HEPATOMA
 HEPATOMA/ HEPATOCELLULAR CARCINOMA
• Keganasan hati, terutama
berhubungan dengan
hepatitis B dan hepatitis C.
• Seringkali tidak bergejala.
Gejala baru timbul di tahap
lanjut, seperti:
– Perut makin membesar
– Nyeri abdomen kanan atas
– Ikterik
– Mudah kenyang
– Penurunan berat badan
– Teraba massa di abdomen
kanan atas
Current diagnosis & treatment in gastroenterology.
• Faktor Risiko: infeksi
hepatitis kronis, aflatoksin,
sirosis
• Gejala
– ↑ɑ-fetoprotein pada > 50%
kasus
– Hati teraba keras, bisa
terdapat nodul
– Adanya bruit atau friction rub
pada perabaan hati
http://emedicine.medscape.com/article/177632-workup#c7
 Penegakan Diagnosis Hepatoma
CT Scan/ MRI abdomen
• Pemeriksaan penunjang inisial
untuk mengetahui adanya
massa/ nodul di hepar.
Biopsi
• Merupakan gold standar
penegakan diagnosis.
• Dilakukan terutama bila
didapatkan nodul >2 cm
Alpha-feto protein (AFP)
• Merupakan tumor marker
untuk hepatoma.
• Dapat false positive pada
kehamilan dan tumor lain yang
berasal dari gonad.
• Digunakan sebagai skrining.
USG
• Dapat digunakan untuk
skrining mengetahui apakah
ada nodul di hepar
• Kombinasi USG dan AFP
memberikan spesifitas yang
tinggi untuk diagnosis
hepatoma.
 Hepatoma
Tata laksana
• Pembedahan/reseksi tumor (bila tumor
mengenai 1 lobus, ukuran < 3 cm)
• Injeksi etanol perkutan dengan tuntunan USG
(bila tumor < 3 buah, ukuran < 3 cm, tumor yang
residif pasca reseksi hati, tumor residual pasca
embolisasi)
• Transplantasi hati
• Kemoembolisasi tumor
• RFA pada tumor <5 cm