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)
• NAFLDmerupakan salah satu kondisi tersering yaitu terdapatnya steatosis
hepatis (fatty liver ),pada org yang tidak mengonsumsi alkohol
/mengonsumsi alkohol < dari 20 g etanol/minggu.
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
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
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.
• 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
• 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%