pemeriksaan fungsi hati
DESCRIPTION
Pemeriksaan Fungsi Hati. dr.Diah Puspita Rini, SpPK. Liver. Biochemycal hepatocyte system: - protein & lipoprotein synthesis - aerob/anaerob metabolism glucose - glycogen synthesis & breakdown - iron & vitamin storage, drug metabolism - synthesis & clearance of hormone - PowerPoint PPT PresentationTRANSCRIPT
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Pemeriksaan Fungsi Hati
dr.Diah Puspita Rini, SpPK
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Liver1. Biochemycal hepatocyte system:
- protein & lipoprotein synthesis- aerob/anaerob metabolism glucose - glycogen synthesis & breakdown- iron & vitamin storage, drug metabolism- synthesis & clearance of hormone
2. Hepatobiliary system: - bilirubin metabolism
3. Reticuloendothelial system:- Kupffer cells
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FUNCTIONS OF THE LIVER• Regulating blood glucose level by making
glycogen, which is stored in hepatocytes.• Synthesizing blood glucose from amino acids of
lactate through gluconeogenesis.• Converting ammonia produced from
gluconeogenetic by-products and bacteria to urea
• Synthesizing plasma proteins such as albumin, globulins, clotting factors, and lipoproteins.
• Breaking down fatty acids into ketone bodies• Storing vitamins and trace metals• Affecting drug metabolism and detoxification• Secreting bile
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Manfaat Tes Fungsi Hati
1. Deteksi penyebab - gangguan fungsi hati - penyakit hati 2. Derajat gangguan fungsi/penyakit hati 3. Evaluasi : Perjalanan Penyakit
Hasil terapi Prognosis
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Keterbatasan TFH
1. Fungsi metabolik hati beragam2. Kapasitas cadangan fungsi hati besar3. Korelasi dg derajat kerusakan hati tidak linier4. Sensitivitas thd kerusakan jar hati tidak sama5. Spesifisitas tidak sama
→ tdk ada tes tunggal yg dpt mendeteksi seluruh penyakit hati
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Macam Tes Fungsi hati1. Tes mengetahui gangguan fungsi
“Uptake” : bilirubin konjugasi : bilirubin ekskresi : bilirubin, asam empedu sintesis : albumin faktor koagulasi
kolinesterase2. Tes integritas sel : AST, ALT, LDH3. Tes kolestasis : Bilirubin, ALP, γ GT, 5’NT4. Tes etiologi
– Marker hepatitis – Tumor marker : CEA, AFP
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BILIRUBIN
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Conjugated bilirubin :1. Water soluble 2. Less toxic to cells 3. Can pass glomerular
filtering membrane
Not found in plasma unless
•Liver cell injury •Obstruction
Then will be found in urine
•Bilirubin dipstick: (+)
- Unconjugated bilirubin :Not water soluble Toxic to cells
–Bound to albumin making it soluble in plasma
–Transported through plasma to liver for excretion
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Gangguan Metabolisme Bilirubin
• Icterus/Jaundice: keadaan yang disebabkan peningkatan bilirubin plasma – Pre hepatik: anemia hemolitik– Hepatik: kerusakan hepatoselular– Post hepatik: batu empedu, tumor pankreas
• Klinis : bila bilirubin total > 2.5mg/dl ICTERUS (JAUNDICE) bila bilirubin unconjugated > 15 mg/dl KERN ICTERUS (terutama pada bayi)
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2
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1
Gangguan metabolisme bilirubin
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Peningkatan Unconjugated Bilirubin
1.Peningkatan produksi: Hemolisis2.Gangguan uptake : sindroma Gilbert’s3. Gangguan konjugasi :
- Neonatal jaundice enzim glukuronil-transferase belum aktif
- penyakit hati yang berat (hepatitis, sepsis)- beberapa macam obat :
*kloramfenikol *pregnanediol breast-milk jaundice - defisiensi glukuronil transferase herediter sindroma Criggler Najjar
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Peningkatan Conjugated Bilirubin
• Kolestasis intra dan ekstra hepatik• Hepatitis, sirosis hepatis• Atresia bilier• Kelainan kongenital, ggn ekskresi:
- Sindroma ROTOR- Sindroma DUBIN-JOHNSON
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Ciri Klinis Hemolitik Hepatoseluler Obstruktif
Warna kulit Kuning pucat Kuning muda-tua kuning
Warna urine normal Gelap Gelap
Warna feses Normal/gelap Pucat (sterkobilin ↓) Warna ≈ dempul
Pruritus - - Menetap
Bilirubin indirek ↑ ↑ ↑
Bilirubin direk N ↑ ↑
Bilirubin urine - ↑ ↑
Urobilinogen urine ↑ Sedikit meningkat ↓
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Analisis Laboratorium Bilirubin
Nilai yang akurat tergantung dari pengambilan dan penanganan spesimen yang benar
Sampel tidak hemolisis (hasil akan rendah palsu karena adanya interference)
Tidak lipemia (lebih utama sampel dalam keadaan puasa)
Light sensitive (cahaya merusak bilirubin)
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• BilirubinTotal : diukur dari kedua macam bilirubin (unconjugated and conjugated)
• Bilirubin Direct : hanya mengukur conjugated bilirubin
• Parameter dihitung : Total – direct = unconjugated (indirect)
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Expected Values: Adults•Total bilirubin: 0.2 – 1.0 mg/dl •Conjugated bilirubin: 0.0 - 0.2 mg/dl •Unconjugated bilirubin: 0.2 – 0.8 mg/dl •Urine bilirubin: negativeExpected Values: Infants
Total bilirubin Premature Full Term 24 hours 1 – 6 mg/dl 2 – 6 mg/dl
48 hours 6 – 8 mg/dl 6 – 7 mg/dl
3-5 days 10 – 12 mg/dl 4 – 6 mg/dl
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FUNGSI SINTESIS HATI
• Sintesis – Total protein – Albumin– Protein koagulasi /faktor koagulasi
• Banyak disintesis di hati• Membutuhkan vitamin K untuk sintesisnya
– Cholinesterase
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Perubahan Fraksi Protein Pada Penyakit Hati
ALBUMIN ↓· Kapasitas cadangan sintesis protein besar, bila Albumin
berarti KERUSAKAN HEPATOSIT LUAS/BERAT· Waktu Paruh albumin : cukup lama ( 20 hr ) bila albumin → kerusakan hepatosit berlangsung
lamaGLOBULIN ↑
terutama globulin- respon terhadap inflamasi - kompensasi
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FAKTOR KOAGULASI PLASMA
disintesis oleh hepatosit - kecuali faktor III,IV,VIII penyakit hati diffus gangguan sintesis faktor koagulasi. sintesis faktor II, VII, IX & X (prothrombin complex) perlu vit K. test : PPT
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Dipengaruhi oleh :- peny.hepatoselular (ggn sintesis)- peny. Obstruktif (ggn absorpsi vit.K)
Protein disintesis di hati
Sintesis membutuhkan vit.K
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CHOLINESTERASE (CHE)
- Penyakit hati kronis, sirosis, hepatitis akut fulminan.- Malnutrisi.- Keracunan insektisida (organofosfat)
AKTIVITAS , SINTESIS NORMAL
Pada hepatitis akut CHE prognosis buruk.
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ENZIM• Protein intraseluler yang dikeluarkan ke
dalam sirkulasi krn adanya kematian /injury sel
• Cardiac enzymes (CK, CK-MB, LD, AST) → IMA• Pancreatic enzymes (amylase, lipase) → pankreatitis• Muscle enzymes (CK, LD, AST) → muscular dystrophy• Bone (ALP) → peny. degeneratif tulang• Liver enzymes (AST, ALT, ALP, GGT)→ peny. liver
• Fungsi: katalisator
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Hepatocyte with cell organelles(schematic representation)and localization of thediagnostically most importantenzymes etc
1. Stellate Kupffer cell2. Space of Disse3. Granular endopl. retic:ChE4. Smooth endopl. retic5. Mitochondrion: GlDH,AST6. Bile canaliculi:ALP,LAP,G-GT7. Nucleus8. Lysosomes :hydrolases9. Cytoplasm:LDH,ALAT,AST Iron
LOKASI ENZIM DALAM HEPATOSIT
ChEAST
ALPGGT
AST,ALT,LDH
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TRANSAMINASE SERUM SGOT : Serum Glutamic Oxaloacetic
Transaminase/AST : ASpartate amino Transferase
→ liver, heart skeletal muscle, kidneys, brain, RBCs half-life 17hrs In liver 20% activity is cytosolic and 80% mitochondrial
SGPT : Serum Glutamic Pyruvic Transaminase/ALT : ALanine amino Transferase
- more specific to liver, very low concentrations in kidney and skeletal muscles.
In liver totally cytosolicHalf-life 47hrs
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AST dan ALT• Dalam sitoplasma hepatosit: - kadar AST 1,5 – 2 x ALT• Pada hepatitis akut:
– AST > ALT– 24-48 jam: kerusakan berlanjut → ALT > AST krn
waktu paruh yg lebih panjang • Kerusakan hati ringan: ALT ↑• Kerusakan hati berat/nekrosis : AST ↑
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Medications causing elevation of aminotransferases
Acetaminophen
Amoxicillin-clavulanic acid
HMGCoA reductase inhbtrs
INH
NSAIDS
Phenytoin
Valproate
Many others
Herbs and toxins• Herbs/alt. medicines• Illicit drugs• Toxins
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RASIO AST/ALT ( de RITIS )
Biasa dipakai bila ada kenaikan transaminase tidak terlalu tinggi < 1 KERUSAKAN HATI AKUT > 1 KERUSAKAN HATI MENAHUN /
SIROSIS• DASAR :
ALT KERUSAKAN MEMBRAN.AST KERUSAKAN ORGANEL +
KERUSAKAN MEMBRAN
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RASIO AST/ALT ( rasio de RITIS )
Biasanya tidak banyak berarti, kecuali bila:
- rasio > 2 : 1 → alkoholic liver disease
- sirosis / hipertensi portal + rasio > 3: primary billiary cirrhosis
- ALT > AST : - viral hepatitis - chronic active hepatitis - cholestasis
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ALP (Alkaline Phosphatase)• Dapat ditemukan:
• Liver• Tulang• Ginjal • Intestine• Placenta
• ALP liver:• Half life 3 hari• Permukaan kanalikuli → disfungsi bilier, ↑ 10x N
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LDH• Terdapat di hampir semua sel• LD isoenzim menunjukkan spesifisitas
jaringanLD-1 (HHHH) LD-2 (HHHM)
Cardiac muscle, kidney, erythrocyte
LD-4 (HMMM) LD-5 (MMMM)
Liver, skeletal muscle
Infark (± 72 jam)Peny. HemolitikSampel lisis
Peny. LiverSkeletal muscle disease
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Gamma-GT• hepatocytes and biliary epithelial cells, pancreas,
renal tubules and intestine• Very sensitive but Non-specific• Raised in ANY liver discease hepatocellular or
cholestatic• Usefulness limited• Confirm hepatic source for a raised ALP• Alcohol• Isolated increase does not require any further
evaluation, suggest watch and repeat only if other LFT’s become abnormal then investigate
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Causes of raised serum gammaglutamyl transferase (GGT)
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INTERPRETASI TFH
• Markers of Hepatocellular damage(Transaminases) :
- AST- ALT
• Markers of Cholestasis:• ALP• Gamma GT• 5’ nucleotidase / 5’NT
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• Bilirubin, Albumin dan Prothrombin time (INR)– Useful indicators of liver synthetic function
– In primary care when associated with liver disease abnormalities should raise concern
– Thrombocytopaenia is a sensitive indicator of liver fibrosis
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Disorder Bilirubin AST/ ALT
ALP Albumin PT
Hemolysis/ Gilberts
unconj ↑ N N N N
Acute hep. cellular ds
Both elevateBilirubin
uria+
ElevateALT > AST
N / < 3 times N
N Usually N
Chronic hep.cellular. ds
Both elevateBilirubin
uria+
Elevate<300u/l
N/ <3 times N
Decrease prolonged
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Disorder Bilirubin AST/ ALT
ALP Albumin PT
Alcohol hepatitis cirrhosis
Both elevate bilirubinuria +
>2 sugg >3 diag
N / <3 times N
↓ prolonged
Obs. jaundice
Both elevate Bilirubinuria+
N to mod elevate
Elevate >4 times N
N unless chronic
N / Prolonged
Infiltrative disease
N N / slight elevate
Elevate >4 times GGT,5’N
N N
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S I R O S I S H A T I Definisi:Penyakit hati yang kronik dan progresif mengakibatkan destruksi dan degenerasi sel parenkim yang extensif
Terdiri dari 4 tipe: Alcoholic (Laennec’s) cirrhosis
→ Associated with alcohol abuse Postnecrotic cirrhosis
→ Complication of toxic or viral hepatitis Biliary cirrhosis
→ Associated with chronic biliary obstruction and infection
Cardiac cirrhosis → Results from longstanding severe right-sided heart failure
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Manifestations of Liver Cirrhosis
Fig. 42-5
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S I R O S I S H A T I COMPENSATED PHASE :
- Gangguan fungsi minimalACTIVE PHASE :
- Nekrosis progresif ( ALT )- Fibrosis kolestasis ( ALP , BILI )
DECOMPENSATED PHASE : - Gangguan fungsi berat
+ hipo albumin + hiperbilirubinemia GAGAL HATI
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SOAL KASUS• Laki-laki 48 th datang dengan keluhan nyeri perut kanan
atas dan febris naik turun selama 3 bulan. Nafsu makan dan BB↓. Dia menderita hepatitis 10 thn y.l. Pemeriksaan fisik: sklera ikterik, hepatomegali 2 cm bac, splenomegali (+)
• Hasil Lab: Hb 9 g /dL WBC 8000/uLPLT 90.000/uLALT 120 U/L (normal < 45) AST 200 U/L (normal < 45)Bilirubin total 10 mg/dl (normal 0,3-1 mg/dl)Bilirubin direk 7,8 mg/dl (normal 0-0,3 mg/dl)HBsAg (+), HBeAg (+), anti-HBc IgM (+)
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a. Apa diagnosis pasien ini?b. Ikterus tipe apa yang dialami oleh pasien
sehingga terjadi peningkatan bilirubin?
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Need a break??
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