Anda di halaman 1dari 110

PEMICU 4

Vivian Saputra
405140126
LO
1. Fatty Liver (alkoholik dan non-alkoholik)
2. Spektrum fatty liver berdasarkan PA
3. Kolesistisis (akut dan kronik)
4. Kolelitiasis
5. Pankreatitis
6. Koledokolitiasis
7. Ca Pankreas
LO 1
FATTY LIVER (ALKOHOLIK DAN NON-ALKOHOLIK)
Perlemakan Hati Non Alkoholik (NAFLD)
• NAFLDmerupakan salah satu kondisi tersering yaitu terdapatnya steatosis
hepatis (fatty liver ),pada org yang tidak mengonsumsi alkohol
/mengonsumsi alkohol < dari 20 g etanol/minggu.

• Merupakan salah 1 penyebab terjadinya chronic liver disease di US.

• Hati  dpt mengalami 3 tipe perubahan (steatosis, steatohepatitis & dapat


menjadi cirrhosis )

• NASH(non alcoholic steatohepatitis)merupakan suatu kondisi dimana


terdapat kerusakan pada hepatosit yang dapat menjadi sirosis(10-20%
kasus)
• NAFLD  berhubungan dengan resistensi insulin & berkaitan dengan
sindrom metabolik.
– Type 2 diabetes (or family history of the condition)
– Obesity (body mass index greater than 30 kg/m2 in whites and
greater than 25 kg/m2 in Asians)
– Dyslipidemia (hypertriglyceridemia, low high-density lipoprotein
cholesterol, high low-density lipoprotein cholesterol)
– Hypertension
• Pada NAFLD Terjadi pe ↑ enzim hati (ALT,AST),jika pasien ada gejala
simtomatik yaitu lelah ,rasa tidak nyaman di RUQ,atau dapat timbul
gejala –gejala chronic liver disease.
• Pasien dengan NASH rata2 asimtomatik tetapi dapat menderita
malaise,lemas /hepatomegali
PATOFISIOLOGI
• Masih belum pasti
• 2 kondisi yang sering dihubungkan yaitu Obesitas dan DM
• 2 abnormalitas metabolik yang berhubungan : peningkatan suplai lemak
ke hati dan resistensi insulin
• Hipotesis yang banyak diterima saat ini adalah The 2 Hit Theory yang
diajukan Day & James
THE TWO HIT THEORY
Penumpukan Lemak di Hepatosit
• FFA diangkut ke hati melalui sirkulasi arteri dan portal
• Di hati FFA dimetabolisme (re-esterifikasi)  Trigliserid / untuk
pembentukan lemak lain
• Pe↑ massa jar.lemak tubuh pada obesitas sentral 
↑pelepasan FFA => penumpukan di hepatosit pe↑ oksidasi &
esterifikasi lemak yang menyebabkan kerusakan mitokondria.
THE TWO HIT THEORY
Stres Oksidatif
• Penyebab : resistensi insulin, ↑ endotoksin di hepar, ↑ aktivitas un-
coupling protein di mitokondria, ↑ aktivitas sitokrom P450 2E1, ↑
cadangan Fe dan ↓aktivitas anti oksidan.
• Stres oksidatif ↑ aktivasi sel stelata & sitokin pro inflamasi 
inflamasi progresif, pembengkakan hepatosit, nekrosis, pembentukan
badan Mallory dan fibrosis.
Manifestasi klinis
• Pasien dengan perlemakan hati non alkoholik tidak menunjukan gejala
/tanda adanya penyakit hati.
• Bbrp pasien menyatakan ada:rasa lemah,malaise,keluhan tidak enak &
sprti mengganjal di perut kanan atas.
• Hepatomegali
Diagnosis

• Biopsi hati  baku emas (gold standard) pemeriksaan


penunjang u/menegakkan diagnosis & metode untuk
membedakan steatosis non alkoholik dengan perlemakan
tanpa /disertai inflammasi
• Careful history (tergantung alkohol yang diminum )
Laboratorium
• Peningkatan ringan sampai sedang ,konsentrasi AST dan ALT /keduanya
 merupakan kelainan hasil pemeriksaan lab yang paling sering
didapat.
• Serum AST dan ALT elevasi 90% pada pasien dengan NASH
• Kenaikan enzim hati tdk melebihi 4x dengan rasio AST : ALT kurang dari
1 ,tetapi pada fibrosis lanjut rasio dapat mendekati /melebihi 1
• Pemeriksaan lab sperti fosfatase alkali ,g-
glutamiltransferase,feritin darah/saturasi transferin juga
dapat meningkat.
• Pada pasien yang sudah menjadi sirosis hipoalbuminemia
,waktu prtrombin yang memanjang dan hiperbilirubinemia.
• Dislipidemia (ditemukan 21%-83% )pasien dan berupa
peningaktan konsentrasi trigliserida.
• Salah 1 faktor resiko perlemakan hati non alkoholik adalah
diabetes terdapat pula peningkatan konsentrasi gula
darah.
Evaluasi Pencitraan
• Ultrasonografi pilihan terbaik saat ini (MRI dan CT scan juga dapat digunakan)
• Pada USG:
– Infiltrasi lemak di hati akan menghasilkan :peningkatan difus ekogenisitas
(hiperekoik ,bright liver )bila dibandingakan dengan ginjal.
• Sensitivitas USG 89% dan spesivisitasnya 93% dalam mendeteksi steatosis.
• Infiltrasi lemak di hati menghasilkan gambar parenkim hati dengan densitas
rendah yang bersifat difus pada CT (adakala bentuk fokal )(sering disalah artikan jdi
massa ganas)
• MRI yang dapat dipakai untuk membedakan nodul karena keganasan dari infiltrasi
fokal di hati.
• NAFLD merupakan suatu spektrum penyakit dari hati
dimulai dari steatosis hepatis ( fatty infiltration of the liver )
sampai menjadi NASH (non alcoholic steatohepatitis )
menjadi cirrhosis
– Fatty infiltration (hepatic steatosis )dari hati abnormalitas yang
sering terjadi karena akumulasi lemak di hepatosit karena (obesitas
,diabetes,hepatitis /cirrhosis )
– Fatty infiltration dapat berupa diffuse/focal & lesi fokal bisa soliter
/multipel
• Jika diffusehepar mengalami pembesaran,pembuluh darah menonjol
mencolok bukan karena obstruksi.
• Gambaran fokal infiltrasi lemak dapat disalahartikan menjadi tumor , tetapi
infiltrasi lemak tidak menimbulkan efek massa & infiltrasi lemak dapat
menghilang dan muncul dalam bbrp minggu.
• MRI merupakan modalitas yang paling akurat dalam evaluasi fatty liver
(fenomena yang disebut chemical shift imaging)
Diffuse fatty liver
Fatty Liver MRI
• Disebut perlemakan hati? jika kandungan lemak dihati (sebagian
besar trigliserida )melebihi 5% dari berat hati.

• Diagnosis dibuat berdasar analisa spesimen biopsi jaringan hati


(ditemukannya min 5-10% sel lemak dari keseluruhan hepatosit)
Gambaran biopsi
• Steatosis
• Infiltrasi sel radang
• Hepatocyte balloning & Nekrosis
• Nukleus glikogen
• Mallory”s hyaline
• Fibrosis (menandakan kerusakan hati lebih lanjut dan lebih berat )
• Karakteristik histologis NAFLD adlh ditemukannya perlemakan hati
dengan/tanpa inflammasi.
– Perlemakan umumnya didominasi o/gambaran sel makrovesikular yang
mendesak inti hepatosit ke tepi sel.
– Pada fase awal /steatosis ringanlemak ditemukan pada zona 3 hepatosit .
– Adanya inflammasi menandakan adanya NASH (sel sel inflamasi terdiri dari
neutrofil dan sel mononuklear yang ada di lobulus hati)(jika sel2 inflammasi tdk
ditemukan berarti pasien dalam tahap perlemakan hati saja )
Grading dan Staging Perlemakan Hati Non
Alkoholik
Grading Steatosis
Grade 1 : <33% hepatosit terisi lemak
Grade 2 : 33 – 66% hepatosit terisi lemak
Grade 3: >66% hepatosit terisi lemak
Grading untuk Steatohepatitis (NASH)
Grade 1 (ringan)
Steatosis : didominasi makrovesikular ,melibatkan hingga 66%
dari lobulus
 Degenerasi balon: kadangkala terlihat: di zona 3 hepatosit
 Inflamasi lobular :inflammasi akut tersebar dan ringan(sel PMN ) kadangkala
inflammasi kronik (sel MN).
 Inflammasi portal: tidak ada/ringan
Grade 2 ,sedang
Steatosis : berbagai derajat,biasanya campuran mikrovesikular dan makrovesikular
Degenerasi balon : jelas terlihat dan terdapat di zona 3
Inflammasi lobular : adanya sel PMN dikaitkan dengan hepatosit yang mengalami
degenerasi ,fibrosis periselular ,inflammasi kronik ringan mungkin ada
Inflammasi portal : ringan –sedang

Grade 3,berat
Steatosis :meliputi >66% lobulus ,umumnya steatosis campuran
Degenerasi :nyata dan terutama dizona 3
Inflammasi lobular: inflammasi akut dan kronik yang tersebar ,sel PMN
terkonsentrasi di area zona 3 yang mengalami degenerasi balon dan fibrosis
perisinusoidal
Inflammasi portal: ringan –sedang
Penatalaksanaan
• Pengobatan lebih ditujukan pada tindakan u/ mengontrol faktor
resiko (spt memperbaiki resistensi insulin & mengurangi asupan
asam lemak ke hati ,baru pemaikan obat)
• Pengontrolan faktor resiko
– Mengurangi BB dengan Diet dan Latihan Jasmani
Tujuan:mengurangi BB (terapi lini pertama bagi NASH),
target penurunan BB adalah u/mengoreksi resistensi
insulin & obesitas sentral.
– Penurunan bb secara bertahap dpt memperbaiki konsentrasi serum
AST dan ALT & gambaran histologi hati NASH.
Latihan jasmani & pengaturan diet terapi dalam usaha mengurangi
berat badan.
Aktivitas fisik berupa latihan bersifat aerobik paling sedikit 30 menit
sehari.
• Esensi pengaturan diet :
– Mengurangi asupan lemak total menjadi <30% dari total asupan energi
– Mengurangi asupan lemak jenuh
– Mengganti dengan karbohidrat kompleks yang mengandung setidaknya 15 gr
serat serta kaya akan buah dan sayuran.
– Mengurangi BB dengan tindakan bedah
Jika gagal dengan pengaturan diet & latihan jasmani
dilakukan operasi bariatrik terhadap pasien dengan perlemakan
hati.
setelah operasi adanya perbaikan pada gambaran histologi hati
tetapi dapat timbul eksaserbasi steatohepatitis pada penurunan bb
yang terlalu cepat.
LO 2
SPEKTRUM FATTY LIVER BERDASARKAN PA
LO 3
KOLESISTISIS (AKUT DAN KRONIK)
ACUTE CHOLECYSTITIS
• Inflammatory response can be evoked by three factors:
(1) Mechanical inflammation produced by increased intraluminal pressure
and distention with resulting ischemia of the gallbladder mucosa and
wall,
(2) Chemical inflammation caused by the release of lysolecithin (due to the
action of phospholipase on lecithin in bile) and other local tissue
factors, and
(3) Bacterial inflammation, which may play a role in 50–85% of patients
with acute cholecystitis.
– The organisms most frequently isolated by culture of gallbladder bile
include Escherichia coli, Klebsiella spp., Streptococcus spp., and
Clostridium spp.
Harrison’s pronciples of internal medicine. 19th ed.
Clinical manifestation
• begins as an attack of biliary pain that progressively worsens
– pain of acute cholecystitis becomes more generalized in the right upper abdomen
– may radiate to the interscapular area, right scapula, or shoulder
• Peritoneal signs of inflammation such as increased pain with jarring or on deep
respiration may be apparent
• The patient is anorectic and often nauseated.
– Vomiting is relatively common
• A low-grade fever is characteristically present, but shaking chills or rigors are not
uncommon
• RUQ of the abdomen is almost invariably tender to palpation
• Deep inspiration or cough during subcostal palpation of the RUQ usually produces
increased pain and inspiratory arrest (Murphy’s sign).
• Localized rebound tenderness in the RUQ is common

Harrison’s pronciples of internal medicine. 19th ed.


Diagnosis
• Usually made on the basis of a characteristic history and physical
examination.
• The triad of sudden onset of RUQ tenderness, fever, and leukocytosis is
highly suggestive.
– Leukocytosis in the range of 10,000–15,000 cells per microliter with a
left shift on differential count is found.
– The serum bilirubin is mildly elevated (<85.5 μmol/L [5 mg/dL]) in fewer
than half of patients,
– Ultrasound will demonstrate calculi in 90–95% of cases and is useful for
detection of signs of gallbladder inflammation including thickening of
the wall, pericholecystic fluid, and dilatation of the bile duct.

Harrison’s pronciples of internal medicine. 19th ed.


pericholecystic fluid

http://reference.medscape.com/features/slideshow/ultrasonography-gallbladder
• Mirizzi’s syndrome is a rare complication
– Which a gallstone becomes impacted in the cystic duct or neck of
the gallbladder  compression of the CBD  CBD obstruction and
jaundice

Harrison’s pronciples of internal medicine. 19th ed.


Treatment acute cholecystitis
• Surgical intervention remains the mainstay of therapy for acute cholecystitis and its
complications.
– Period of in-hospital stabilization may be required before cholecystectomy.
• Oral intake is eliminated,
• Nasogastric suction may be indicated, and
• Extracellular volume depletion and electrolyte abnormalities are repaired
• Meperidine or nonsteroidal anti-inflammatory drugs (NSAIDs)  for analgesia because
they may produce less spasm of the sphincter of Oddi than drugs such as morphine.
• Intravenous antibiotic therapy  patients with severe acute cholecystitis, even though
bacterial superinfection of bile may not have occurred in the early stages of the
inflammatory process.

Harrison’s pronciples of internal medicine. 19th ed.


Treatment acute cholecystitis
• Antibiotic therapy
– most common organisms likely to be present : E. coli, Klebsiella spp., and
Streptococcus spp
– Effective antibiotics include ureidopenicillins, spt:
• piperacillin or mezlocillin,
• ampicillin sulbactam,
• ciprofloxacin,
• moxifloxacin, and
• third-generation cephalosporins
– Anaerobic coverage by a drug (metronidazole) should be added  if gangrenous or
emphysematous cholecystitis is suspected.

Harrison’s pronciples of internal medicine. 19th ed.


Treatment acute cholecystitis
• Surgical therapy
– Depends on stabilization of the patient.
– Urgent (emergency) cholecystectomy or cholecystostomy  u/ psn yg ad
komplikasi (spt: empyema, emphysematous cholecystitis, or perforation is
suspected or confirmed)
– Patients with uncomplicated acute cholecystitis  early elective
laparoscopic cholecystectomy  ideally within 48–72 h after diagnosis
– Thus, early cholecystectomy (within 72 h) is the treatment of choice for
most patients with acute cholecystitis

Harrison’s pronciples of internal medicine. 19th ed.


Chronic cholecystitis
• Chronic cholecystitis is swelling and irritation of the gallbladder that
continues over time.
• Causes:
– Most of the time, chronic cholecystitis is caused by repeated attacks
of acute (sudden) cholecystitis.
– Most of these attacks are caused by gallstones in the gallbladder.
– These attacks cause the walls of the gallbladder to thicken. The
gallbladder begins to shrink. Over time, the gallbladder is less able
to concentrate, store, and release bile.

https://medlineplus.gov/ency/article/000217.htm
Exam & test
• our health care provider may order the following blood tests:
– Amylase and lipase. To diagnose diseases of the pancreas.
– Complete blood count (CBC)
– Liver function tests. To evaluate how well the liver is working.
• Tests that reveal gallstones or inflammation in the gallbladder
include:
– Abdominal CT scan
– Abdominal ultrasound
– Gallbladder scan (HIDA scan)
– Oral cholecystogram

https://medlineplus.gov/ency/article/000217.htm
Treatment Chronic cholecystitis
• Surgery is the most common treatment. Surgery to remove the
gallbladder is called cholecystectomy.
– Laparoscopic cholecystectomy is most often done.
• This surgery uses smaller surgical cuts, which result in a faster
recovery. Many people are able to go home from the hospital on
the same day as surgery, or the next morning.
– Open cholecystectomy requires a larger cut in the upper-right part
of the abdomen.

https://medlineplus.gov/ency/article/000217.htm
Complication
• Empyema and hydrops
– Empyema usually results from progression of acute cholecystitis with persistent
cystic duct obstruction to superinfection of the stagnant bile with a pus-forming
bacterial organism.
– Empyema of the gallbladder carries a high risk of gram-negative sepsis and/or
perforation.
– Hydrops or mucocele of the gallbladder may also result from prolonged obstruction of
the cystic duct, usually by a large solitary calculus
• he obstructed gallbladder lumen is progressively distended, by mucus (mucocele)
or by a clear transudate (hydrops) produced by mucosal epithelial cells.
• Cholecystectomy is indicated, because empyema, perforation, or gangrene may
complicate the condition.

Harrison’s pronciples of internal medicine. 19th ed.


Complication
• Gangrene and perforation
– Gangrene of the gallbladder results from ischemia of the wall and patchy or complete
tissue necrosis.
• Underlying conditions often include marked distention of the gallbladder,
vasculitis, diabetes mellitus, empyema, or torsion resulting in arterial occlusion.
– Gangrene  presidposes to perforation, but perforation may also occur in chronic
cholecystitis.(tanpa tanda gejala)
• Localized perforations  contained by the omentum or by adhesions produced by
recurrent inflammation of the gallbladder.
• Bacterial superinfection of the walled-off gallbladder contents results in abscess
formation
• Most patients are best treated with cholecystectomy, but some seriously ill
patients may be managed with cholecystostomy and drainage of the abscess.

Harrison’s pronciples of internal medicine. 19th ed.


Complication

• Fistula formation and gallstone ileus


– Fistula formation into an adjacent organ adherent to the gallbladder
wall may result from inflammation and adhesion formation.
• Fistulas into the duodenum are most common, followed in
frequency by those involving the hepatic flexure of the colon,
stomach or jejunum, abdominal wall, and renal pelvis
– Gallstone ileus refers to mechanical intestinal obstruction resulting from
the passage of a large gallstone into the bowel lumen
• Msk lewat cholecystoenteric fistula .
• Tempat sumbatan biasanya ileocecal valve.

Harrison’s pronciples of internal medicine. 19th ed.


LO 4
KOLELITIASIS
LO 5
PANKREATITIS
Pankreatitis
• Penyakit peradangan pankreas diklasifikasikan sebagai pankreatitis
akut dan kronik.
• Spektrum patologik pankreatitis akut berkisar dari pankreatitis
interstisialis (yang biasanya ringan) sampai pankreatitis nekrotikans (yg
derajat nekrosis pankreas berkorelasi dengan keparahan serangan dan
manifestasi sistemiknya).
• Insidens pankreatitis bervariasi tergantung penyebabnya.
• Insidens di Inggris ± 5,4/100.000 per tahun dan di Amerika Serikat ±
79,8/100.000 per tahun.
Pankreatitis Akut
– Proses peradangan akut yang mengenai pankreas dan ditandai oleh
nyeri perut yang akut disertai kenaikan enzim dalam darah dan urin.
– Ditandai dengan onset nyeri abdomen yang mendadak, mual, dan
muntah.
– 85%-90% pankreatitis akut  gejala pulih dalam 3 – 7 hari setelah
mulai pengobatan
Pankreatitis Akut
ETIOLOGI
Kausa Umum Kausa tak umum
• Batu empedu (termasuk mikrolitiasis) • Kausa vaskular & vaskulitis (keadaan iskemia-
• Alkohol (alkoholisme akut dan kronik) hipoperfusi setelah bedah jantung)
• Hipertriliseridemia • Penyakit jaringan ikat dan purpura
• Endoscopic retrograde trombositopenik trombotik
cholangiopancreatography (ERCP), • Kanker pankreas
khususnya setelah manometri biliaris • Hiperkalsemia
• Trauma (terutama trauma tumpul • Divertikulum periampula
abdomen) • Pankreas divisum
• Pascaoperasi (operasi abdomen & non- • Pankreatitis herediter
abdomen) • Fibrosis kistik
• Obat (azatioprin, 6-merkaptopurin, • Gagal ginjal
sulfonamid, estrogen, tetrasiklin, asam
valproat, obat anti- HIV) Kausa yang jarang
• Disfungsi sfingter Oddi
• Infeksi (gondongan, coxsackie virus,
sitomegalovirus, ekovirus, parasit)
• Autoimun (mis Sindrom Sjogren)
Pankreatitis Akut
ETIOLOGI
• Batu empedu  penyebab utama pankreatitis akut (30-60%)
• Alkohol  penyebab tersering ke 2 (15-30%)
• Hipertrigliseridemia  penyebab pankreatitis akut pada 1,3-3,8%
kasus, kadar trigliserida serum biasanya >11,3 mmol/L
• Pasien setelah ERCP  5-20%
• Pankreatitis akut berkaitan dengan obat  2-5%
Kumar V, Abbas AK, Fausto N, Aster JC.
Robbins and cotran pathologic basis of
disease. 9th ed. Philadelphia: Saunders
Patogenesis Pankreatitis
• Autodigesti  salah satu teori patogenik dengan pankreatitis terjadi
jika enzim- enzim proteolitik (tripsinogen, kimotripsinogen,
proelastase, dan fosfolipase A) diaktifkan di pankreas bukan di lumen
usus
• Endotoksin, eksotoksin, infeksi virus, iskemia, anoksia, trauma
langsung) dipercaya dapat mengaktifkan proenzim tsb.
• Enzim” proteolitik yg sudah aktif khususnya tripsin, tidak hanya
mencerna jaringan pankreas & peripankreas tapi juga bisa
mengaktifkan enzim lain.
Patogenesis Pankreatitis Akut
Terdiri dari 3 fase :
• Fase awal
ditandai oleh pengaktifan enzim pencernaan intrapankreas & cedera
sel asinus. Pengaktifan zimogen tampaknya diperantarai oleh hidrolase
lisosom misalnya katepsin B yang terlokalisasi bersama enzim”
pencernaan di organel intrasel.

• Fase kedua
melibatkan pengaktifan, kemoatraksi, dan sekuestrasi neutrofil di
pankreas yg menyebabkan reaksi peradangan intrapankreas dengan
keparahan bervariasi.
Patogenesis Pankreatitis Akut
• Fase ketiga
terjadi karena efek berbagai enzim proteolitik yang telah aktif serta
sitokin yang terbebaskan oleh pankreas yang meradang.
- Enzim proteolitik aktif terutama tripsin tidak saja mencerna jaringan
pankreas dan peripankreas tapi juga mengaktifkan enzim lain (elastase
dan fosfolipase)
- Enzim” tsb akan mencerna membran sel  proteolisis, edema,
perdarahan interstitium, kerusakan vaskular, nekrosis koagulasi, lemak
dan sel parenkim.
- Cedera & kematian sel menyebabkan pembebasan peptida bradikinin,
bahan” vasoaktif, & histamin  vasodilatasi, peningkatan
permeabilitas vaskular & edema.
Townsend CM, Beauchamp RD, Evers BM, Mattox KL. Sabiston textbook
of surgery: the biological basis of modern surgical practice. 19th ed.
Philadelphia: Saunders Elsevier; 2012.
Townsend CM, Beauchamp RD, Evers BM, Mattox
KL. Sabiston textbook of surgery: the biological
basis of modern surgical practice. 19th ed.
Philadelphia: Saunders Elsevier; 2012.
Tanda dan Gejala Pankreatitis Akut
• Nyeri abdomen  biasanya memiliki karakter tetap dan tumpul,
terletak di daerah epigastrium & periumbilikalis, sering menyebar ke
punggung serta dada, pinggang & abdomen bawah
• Mual
• Muntah
• Demam ringan
• Hipertensi ringan
Townsend CM, Beauchamp RD, Evers BM, Mattox
KL. Sabiston textbook of surgery: the biological
basis of modern surgical practice. 19th ed.
Philadelphia: Saunders Elsevier; 2012.
Klasifikasi Pankreatitis Akut
Pankreatitis akut tipe interstitial Pankreatitis akut tipe nekrosis
Nekrosis lemak di tepi pankreas Nekrosis setempat / difus
Edema interstitial, ringan & self Disertai pendarahan / inflamasi
limited
Secara makroskopik pankreas
membengkak secara difus dan
tampak pucat
Tidak didapatkan perdarahan atau
nekrosis, atau bila ada minim sekali
Pemeriksaan Fisik Pankreatitis Akut
• Tidak nyaman dalam posisi • Nodus” eritematosa di kulit
telentang • Efusi pleura
• Nyeri tekan midepigastrium • Cullen’s sign : diskolorasi biru
• Massa pada palpasi abdomen samar di sekitar umbilikus
atas dapat terjadi akibat
• Busing usus : lenyap / ↓ hemoperitoneum
• Kadang ikterus • Turner’s sign : diskolorasi biru-
merah-ungu atau hijau-coklat
• Distensi abdomen ringan di pinggang  katabolisme di
jaringan
Pemeriksaan Laboratorium Pankreatitis
Akut
• Amilase serum meningkat ( ↑ • Enzim hati dan bilirubin ↑
3xN ) (bilirubin serum >68 μmol/ L
• Lipase serum meningkat pada 10% pasien)
• Hitung leukosit ↑ (15.000- • Kadar glukosa plasma ↑
20.000) • Kalsium plasma ↓
• Hb dan Ht dapat ↑/↓ • kadar fosfatase alkali dan
• Nitrogenurea dan kreatinin aspartat aminotransferase ↑
darah ↑ • LDH ↑ (> 8,5 μmol/L =
prognosis buruk)
Diagnosis Banding
• Perforase viskus, terutama tukak peptik
• Kolesistitis akut & kolik empedu
• Obstruksi usus halus
• Oklusi vaskular mesenterium
• Kolik ginjal
• Infark miokardium
• Aneurisma aorta disekans
• Gangguan jaringan ikat
• Pneumonia
• Ketoasidosis diabetes
Terapi Suportif Pankreatitis Akut
• Mengistirahatkan kelenjar yang sakit
– pasien dipuasakan, pemasangan sonde sangat dianjurkan
– mengurangi rangsang saraf dan hormon dari pankreas eksokrin
– penyingkiran asam lambung dan pengurangan distensi lambung
– mencegah aspirasi karena muntah
– pemberian analgesik (mengurangi rangsangan saraf yang diinduksi
oleh stres atas sekresi lambung dan pankreas)
Terapi Suportif Pankreatitis Akut
• Mencegah kemungkinan komplikasi
– pemberian antibiotika ( untuk resiko sepsis tinggi )
– antasid (mengurangi pengeluaran asam lambung ke duodenum dan
resiko perdarahan sekunder terhadap gastritis / duodenitis)
– pemberian cairan intravena ( untuk mengatsi hipokalsemi dan
hindari gagal ginjal dan kolaps sirkulasi )
– untuk memperoleh gizi yang cukup  alimenterasi parenteral

• Bantuan pernafasan ( hipoksia, infiltrat paru )


Terapi Bedah Pankreatitis Akut
• Indikasi :
– Diagnosis definitif pankreatitis belum dibuat
– Tanda bahaya pada abdomen atas menetap
– Komplikasi (abses/kista) atau faktor etiologi memerlukan
intervensi bedah
– Kasus pankreatitis akuta yang meyertai batu empedu

• Tindakan :
– Bilas peritoneum
– Drainase luas (reseksi atau debridement kelenjar nekrotik)
– Kolesistostomi, kolesistektomi / dekompresi duktus komunis
PANKREATITIS AKUT
• Komplikasi • Prognosis:
– Diabetes melitus – 85-90% penderita
– Tetani hebat pankreatitis akut, gejala
biasanya pulih dalam 3
– Efusi pleura hingga 7 hari setelah mulai
– Abses pankreas pengobatan
– Pseudokista pankreas – Mortalitas pankreatitis akut
10%
– Mortalitas pankreatitis
nekrotik berat adalah 50%
– Pembedahan tampaknya
dapat menurunkan angka
kematian
PANKREATITIS KRONIS
Definitions
• irreversible damage to pancreas
characterized by:
(1) pancreatic cell loss (from necrosis)
(2) inflammation
(3) fibrosis
Etiology
• alcohol (most common): • unusual causes
– causes a larger proportion (>90%) of
chronic pancreatitis than acute – cystic fibrosis
pancreatitis – severe protein-calorie
– changes composition of pancreatic juice malnutrition
(e.g. increases viscosity)
– decreases pancreatic secretion of – hereditary
pancreatic stone protein (lithostathine)
which normally solubilizes calcium salts
• precipitation of calcium within
pancreatic duct results in duct and
gland destruction
– toxic effect on acinar and duct cells –
directly or via increasing free radicals
– acinar cell injury leads to cytokine
release, which stimulates pancreatic
stellate cells to form collagen (leading to
fibrosis)
Kumar V, Abbas AK, Fausto N, Aster JC.
Robbins and cotran pathologic basis of
disease. 9th ed. Philadelphia: Saunders
Signs and symptoms
• early stages:
– recurrent attacks of severe abdominal pain (upper abdomen and
back)
– chronic painless pancreatitis: 10%

• late stages: occurs in 15% of patients


– malabsorption syndrome when >90% of function is lost, steatorrhea
– diabetes, calcification, jaundice, weight loss, pseudocyst, ascites, GI
bleed
Investigations
• laboratory:
– increase in serum glucose
– increase in serum ALP, less commonly bilirubin (jaundice)
– serum amylase and lipase usually normal
• AXR: looking for pancreatic calcifications
• U/S or CT: calcification, dilated pancreatic ducts, pseudocyst
• MRCP or ERCP: abnormalities of pancreatic ducts-narrowing and dilatation
• EUS: abnormalities of pancreatic parenchyma and pancreatic ducts
• 72-h fecal fat test: measures exocrine function
• secretin test: gold standard, measures exocrine function but difficult to perform,
unpleasant for patient, expensive
• fecal pancreatic enzyme measurement (elastase-1, chymotrypsin) available only in
selected centres
Investigations
• best imaging modality: MRCP
• findings: U/S, CT scan and MRI may show calcifications, ductal
dilatation, enlargement of the pancreas and fluid collections (e.g.
pseudocysts) adjacent to the gland. However, magnetic resonance
cholangiopancreatography (MRCP) is becoming the diagnostic test of
choice since it can show calcification and pancreatic duct obstruction
Management
• most common problem is pain, difficult to control
• general management:
– total abstinence from alcohol
– enzyme replacement may help pain by resting pancreas via negative
feedback
– analgesics
– celiac ganglion blocks
– time: pain decreases with time as pancreas “burns out”
• endoscopy: sphincterotomy, stent if duct dilated, remove stones from
pancreatic duct
Management
• surgery: drain pancreatic duct (pancreaticojejunostomy) if duct dilated
(more effective than endoscopy); resect pancreas if duct contracted
• steatorrhea:
– pancreatic enzyme replacement
– restrict fat, increase carbohydrate and protein (may also decrease
pain)
– neither endoscopy nor surgery can improve pancreatic function
Surgical treatment
• treatment is generally medical
• indications for surgery:
– failure of medical treatment
– debilitating abdominal pain
– pseudocyst complications: persistence, hemorrhage, infection, rupture
– CBD obstruction (e.g. strictures), duodenal obstruction
– pancreatic fistula, variceal hemorrhage secondary to splenic vein obstruction
– rule out pancreatic cancer (present in 15% of chronic pancreatitis treated surgically)
– anatomical abnormality causing recurrent pancreatitis
• pre-op CT and/or ERCP are mandatory to delineate anatomy
• minimally invasive options:
– endoscopic pancreatic duct decompression: less effective than surgery
– extracorporeal shockwave lithotripsy: if pancreatic duct stones
– celiac plexus block: lasting benefit in 30% patients, less effective in those <45 yr or with prior
pancreatic surgery
Surgical treatment
• surgical options:
– drainage procedures: only effective if ductal system is dilated
• Puestow procedure (lateral pancreaticojejunostomy): improves pain in 80%
of patients
– pancreatectomy: best option in absence of dilated duct
• proximal disease: Whipple procedure (pancreaticoduodenectomy) – pain
relief in 80%
• distal disease: distal pancreatectomy ― Roux-en-Y pancreaticojejunostomy
• total pancreatectomy: refractory disease
– denervation of celiac ganglion and splanchnic nerves
• pseudocyst (often resolve spontaneously with pancreatic rest):
– cyst wall must be mature prior to drainage (4-6 wk)
– pseudoaneurysm an absolute contraindication to endoscopic drainage, must
embolize first
– percutaneous catheter drainage
Surgical treatment
– surgical drainage (gold standard):
• cystgastrostomy
• cystenterostomy
• resection
– endoscopic drainage:
• cystgastrostomy
• cystduodenostomy
– consider biopsy of cyst wall to rule out cystadenocarcinoma
LO 6
KOLEDOKOLITIASIS
CHOLEDOCHOLITHIASIS
• Definisi:
– Passage of gallstones into the CBD (common bile duct).
– Occurs in ∼10–15% of patients with cholelithiasis.
• Epidemiologi:
– The incidence of common duct stones increases with
increasing age of the patient,
• Up to 25% of elderly patients may have calculi in the common
duct at the time of cholecystectomy.

Harrison’s pronciples of internal medicine. 19th ed.


http://nurseslabs.com/choledocolithiasis-pathophysiology-schematic-diagram/
http://nurseslabs.com/choledocolithiasis-pathophysiology-schematic-diagram/
Risk factor
• CBD stones should be suspected in gallstone patients who
have any of the following risk factors:
(1) A history of jaundice or pancreatitis,
(2) Abnormal tests of liver function, and
(3) Ultrasonographic or MRCP evidence of a dilated CBD or stones in
the duct
Diagnosis
• The diagnosis of choledocholithiasis is usually
made by cholangiography, either:
– preoperatively by endoscopic retrograde cholangiogram
(ERC) or
– MRCP or intraoperatively at the time of
cholecystectomy

Harrison’s pronciples of internal medicine. 19th ed.


Harrison’s pronciples of internal medicine. 19th ed.
Harrison’s pronciples of internal medicine. 19th ed.
Harrison’s pronciples of internal medicine. 19th ed.
Treatment
• When CBD stones are suspected prior to laparoscopic cholecystectomy,
preoperative ERCP with endoscopic papillotomy and stone extraction
is the preferred approach

Harrison’s pronciples of internal medicine. 19th ed.


Complication
• Cholangitis (1)
– may be acute or chronic, and symptoms result from inflammation, which
usually is caused by at least partial obstruction to the flow of bile
– The characteristic presentation of acute cholangitis involves:
• biliary pain, jaundice, and spiking fevers with chills (Charcot’s triad).
• Blood cultures are frequently positive, and leukocytosis is typical.
– Nonsuppurative acute cholangitis is most common and may respond
relatively rapidly to supportive measures and to treatment with antibiotics

Harrison’s pronciples of internal medicine. 19th ed.


Complication
• Cholangitis(2)
– suppurative acute cholangitis  the presence of pus under pressure in a
completely obstructed ductal system leads to symptoms of severe toxicity—
mental confusion, bacteremia, and septic shock.
• Response to antibiotics alone in this setting is relatively poor,
• multiple hepatic abscesses are often present, and
• the mortality rate approaches 100% unless prompt endoscopic or
surgical relief of the obstruction and drainage of infected bile are carried
out.
• ERCP with endoscopic sphincterotomy is safe and the preferred initial
procedure for both establishing a definitive diagnosis and providing
effective therapy

Harrison’s pronciples of internal medicine. 19th ed.


Complication
• Obstructive jaundice
– Gradual obstruction of the CBD (weeks or months)  initial manifestations
of jaundice or pruritus without associated symptoms of biliary colic or
cholangitis.
– CBD stones should be suspected in any patient with cholecystitis whose
serum bilirubin level is >85.5 μmol/L (5 mg/dL)
• Maximum bilirubin level is seldom >256.5 μmol/L (15.0 mg/dL) 
unless concomitant hepatic or renal disease or another factor leading
to marked hyperbilirubinemia exists.
• Serum bilirubin levels ≥342.0 μmol/L (20 mg/dL) should suggest the
possibility of neoplastic obstruction.
– The serum alkaline phosphatase level is almost always elevated in biliary
obstruction
Harrison’s pronciples of internal medicine. 19th ed.
Complication
• Pancreatitis
– The most common associated entity discovered in patients
with nonalcoholic acute pancreatitis is biliary tract disease.
– Biochemical evidence of pancreatic inflammation complicates
acute cholecystitis in 15% of cases and choledocholithiasis in
>30%
• the common factor appears to be the passage of gallstones through
the common duct.
– Surgical treatment of gallstone disease is usually associated
with resolution of the pancreatitis.

Harrison’s pronciples of internal medicine. 19th ed.


Complication

• Secondary biliary cirrhosis


– may complicate prolonged or intermittent duct obstruction with or
without recurrent cholangitis.
– More common in cases of prolonged obstruction from stricture or
neoplasm.

Harrison’s pronciples of internal medicine. 19th ed.


LO 7
CA PANKREAS
Kanker Pankreas

• Tumor pankreas dapat berasal dari jaringan eksokrin dan endokrin


• 90% adalah tumor ganas yang berasal dari jaringan eksokrin yaitu
adenokarsinoma duktus pankreas
• Di bagi menjadi :
– tipe obstruksi  caput pankreas
– non-obstruksi  corpus dan cauda
Epidemiologi
• Insidensi meningkat seiring bertambahnya usia
• 80% usia 60-80 tahun
• Pria > Wanita  1,2 - 1,5 : 1
• 98% pasien meninggal
• 70 % di caput pankreas
• Insidens lebih tinggi pada orang Amerika Afrika daripada Kaukasus
Etiologi
• Faktor eksogen
– Kebiasaan merokok  faktor resiko paling konsisten
 1,4 – 2,3 kali lebih tinggi
– Diet tinggi lemak
– Alkohol
– Kopi
– Zat karsinogen Industri
• Faktor endogen
– Usia
– Pankreatitis kronik  9,5 kali
– DM kronik
• Faktor genetik
Gambaran Klinik
• Yg umum ditemukan • Yg kadang ditemukan
– BB turun tanpa sebab yg – Obstruksi pylorus/duodenum
jelas karena tekanan dari luar
– Nyeri perut – Tromboflebitis ringan
– Ikterus obstruksi – Pankreatitis akut
– anoreksia – Perdarahan GI (erosi duodenum)
– Steatorea ( obstruksi dikus
pankreatikus)
– DM
Tipe Obstruksi
• Terjadi di bagian caput pankreas
• Gambaran klinis :
– Tdk bergejala/bertanda sampai tjd ikterus obstruksi
– Menurunnya berat badan
– Nyeri epigastrium
– Massa di epigastrium
– Nyeri hebat di punggung pd 25% pasien
– Kandung empedu  tdk nyeri saat di tekan
– Ikterus
– Pruritus
– Kolangitis
Tipe Nonobstruksi
• Terjadi pada bagian corpus dan cauda pankreas
• Gejala klinis
– BB turun
– Nyeri di epigastrium dan pinggang
– Hepatomegali
Staging
• The American Joint Committee on Cancer (AJCC) tumor-node-
metastasis (TNM) staging of pancreatic cancer takes into
account the location and size of the tumor, the involvement of
lymph nodes, and distant metastasis.
Pemeriksaan
• Pemeriksaan Laboratorium
– Kadar billirubin serum  tdk pernah lebih dari 30-35 mg/L
– Fosfatase alkali selalu meningkat  blm ada ikterus
– Transaminase serum < 500 U/I
Pemeriksaan pencitraan
– Foto polos  perubahan bentuk duodenum  angka 3 terbalik 
penekanan ke dlm duodenum, melebarnya lengkung duodenum, dan
kardia lambung terdorong ke kranial
– Kolangipankreatiografi endoskopik retrogard  bendungan dan
bayangan iregular saluran pankreas
– USG  menentukan letak dan besarnya tumor, pelebaran saluran
pankreas dan empedu
– CT scan  diagnosis tumor dan invasi ke organ lainnya
– Kolangiografi transhepatik perkutan  bila ada ikterus obstruksi
– Biopsi
• Petanda tumor CEA dan Ca 19-9
– Dianggap paling baik untuk diagnosis kanker pankreas
– Sensitivitas dan spesivisitas: 80% dan 60-70%
– Konsentrasi tinggi terdapat pada pasien dngan besar tumor ≥ 3 cm
• MRI: untuk evaluasi kanker
Penatalaksanaan
• Terapi bedah
– Operasi Wipple  tumor yg msh terlokalisasi (sekitar
ampula vater, duodenum, duktus koledokus distal)
– Pembedahan Paliatif  karsinoma pankreas yg sdh tdk
bisa direseksi lagi krna invasi keluar hulu pankreas atau
metastasis limfe
Prognosis
• Penderita yg mendapat terapi bedah kuratif  harapan hidup
1, 2, dan 5 tahun
• Penderita yg tdk mendapat terapi bedah kuratif  harapan
hidup 6 bulan

Anda mungkin juga menyukai