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Pemeriksaan Fungsi Hati dr.Diah Puspita Rini, SpPK.

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Presentasi berjudul: "Pemeriksaan Fungsi Hati dr.Diah Puspita Rini, SpPK."— Transcript presentasi:

1 Pemeriksaan Fungsi Hati dr.Diah Puspita Rini, SpPK

2 Liver 1.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

3 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

4 Manfaat Tes Fungsi Hati 1. Deteksi penyebab - gangguan fungsi hati - gangguan fungsi hati - penyakit hati - penyakit hati 2. Derajat gangguan fungsi/penyakit hati 3. Evaluasi : Perjalanan Penyakit Hasil terapi Hasil terapi Prognosis Prognosis

5 Keterbatasan TFH 1.Fungsi metabolik hati beragam 2.Kapasitas cadangan fungsi hati besar 3.Korelasi dg derajat kerusakan hati tidak linier 4.Sensitivitas thd kerusakan jar hati tidak sama 5.Spesifisitas tidak sama → tdk ada tes tunggal yg dpt mendeteksi seluruh penyakit hati

6 Macam Tes Fungsi hati 1. Tes mengetahui gangguan fungsi “Uptake” : bilirubin konjugasi : bilirubin ekskresi : bilirubin, asam empedu sintesis : albumin faktor koagulasi kolinesterase 2. Tes integritas sel : AST, ALT, LDH 3. Tes kolestasis : Bilirubin, ALP, γ GT, 5’NT 4. Tes etiologi –Marker hepatitis –Tumor marker : CEA, AFP

7 BILIRUBIN

8 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

9 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)

10 Gangguan metabolisme bilirubin

11 Peningkatan Unconjugated Bilirubin 1.Peningkatan produksi: Hemolisis 2.Gangguan uptake : sindroma Gilbert’s 3. Gangguan konjugasi : -Neonatal jaundice  enzim glukuronil-transferase belum aktif -penyakit hati yang berat (hepatitis, sepsis) -beberapa macam obat : *kloramfenikol breast-milk jaundice *pregnanediol  breast-milk jaundice - defisiensi glukuronil transferase herediter  sindroma Criggler Najjar

12 Peningkatan Conjugated Bilirubin Kolestasis intra dan ekstra hepatik Hepatitis, sirosis hepatis Atresia bilier Kelainan kongenital, ggn ekskresi: -Sindroma ROTOR -Sindroma DUBIN-JOHNSON

13 Ciri KlinisHemolitikHepatoselulerObstruktif Warna kulitKuning pucatKuning muda-tuakuning Warna urinenormalGelap Warna fesesNormal/gelapPucat (sterkobilin ↓) Warna ≈ dempul Pruritus--Menetap Bilirubin indirek ↑↑↑ Bilirubin direkN ↑↑ Bilirubin urine- ↑↑ Urobilinogen urine ↑ Sedikit meningkat ↓

14 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)

15 BilirubinTotal : diukur dari kedua macam bilirubin (unconjugated and conjugated) Bilirubin Direct : hanya mengukur conjugated bilirubin Parameter dihitung : Total – direct = unconjugated (indirect)

16 Expected Values: Adults Total bilirubin: 0.2 – 1.0 mg/dl Conjugated bilirubin: mg/dl Unconjugated bilirubin: 0.2 – 0.8 mg/dl Urine bilirubin:negative Expected Values: Infants Total bilirubinPrematureFull Term 24 hours1 – 6 mg/dl2 – 6 mg/dl 48 hours6 – 8 mg/dl6 – 7 mg/dl 3-5 days10 – 12 mg/dl4 – 6 mg/dl

17 FUNGSI SINTESIS HATI Sintesis –Total protein –Albumin –Protein koagulasi /faktor koagulasi Banyak disintesis di hati Membutuhkan vitamin K untuk sintesisnya –Cholinesterase

18 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 lama GLOBULIN ↑ terutama  globulin  - respon terhadap inflamasi - kompensasi

19 19 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

20 Dipengaruhi oleh : - peny.hepatoselular (ggn sintesis) - peny. Obstruktif (ggn absorpsi vit.K) Protein disintesis di hati Sintesis membutuhkan vit.K

21 CHOLINESTERASE (CHE)  -Penyakit hati kronis, sirosis, hepatitis akut fulminan. -Malnutrisi. -Keracunan insektisida (organofosfat)  AKTIVITAS, SINTESIS NORMAL Pada hepatitis akut   CHE     prognosis buruk.

22 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

23 23 Hepatocyte with cell organelles (schematic representation) and localization of the diagnostically most important enzymes etc 1. Stellate Kupffer cell 2. Space of Disse 3. Granular endopl. retic:ChE 4. Smooth endopl. retic 5. Mitochondrion: GlDH,AST 6. Bile canaliculi:ALP,LAP,G-GT 7. Nucleus 8. Lysosomes :hydrolases 9. Cytoplasm:LDH,ALAT,AST Iron LOKASI ENZIM DALAM HEPATOSIT ChE AST ALP GGT AST,ALT,LDH

24 24 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 cytosolic Half-life 47hrs

25 25 AST dan ALT Dalam sitoplasma hepatosit:Dalam sitoplasma hepatosit: - kadar AST 1,5 – 2 x ALT - kadar AST 1,5 – 2 x ALT Pada hepatitis akut:Pada hepatitis akut: –AST > ALT –24-48 jam: kerusakan berlanjut → ALT > AST krn waktu paruh yg lebih panjang Kerusakan hati ringan: ALT ↑Kerusakan hati ringan: ALT ↑ Kerusakan hati berat/nekrosis : AST ↑Kerusakan hati berat/nekrosis : AST ↑

26 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

27 27 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

28 28 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

29 ALP (Alkaline Phosphatase) Dapat ditemukan: Liver Tulang Ginjal Intestine Placenta ALP liver: Half life 3 hari Permukaan kanalikuli → disfungsi bilier, ↑ 10x N

30

31 LDH Terdapat di hampir semua sel LD isoenzim menunjukkan spesifisitas jaringan LD-1 (HHHH) LD-2 (HHHM) Cardiac muscle, kidney, erythrocyte LD-4 (HMMM) LD-5 (MMMM ) Liver, skeletal muscle Infark (± 72 jam) Peny. Hemolitik Sampel lisis Peny. Liver Skeletal muscle disease

32 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

33 Causes of raised serum gammaglutamyl transferase (GGT)

34 34 INTERPRETASI TFH Markers of Hepatocellular damage (Transaminases) : - AST - ALT Markers of Cholestasis: ALP Gamma GT 5’ nucleotidase / 5’NT

35 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

36 DisorderBilirubinAST/ ALT ALPAlbuminPT Hemolysis / Gilberts unconj ↑ NNNN Acute hep. cellular ds Both elevate Bilirubin uria+ Elevate ALT > AST N / < 3 times N NUsually N Chronic hep. cellular. ds Both elevate Bilirubin uria+ Elevate <300u/l N/ <3 times N Decreaseprolonged

37 DisorderBilirubinAST/ ALT ALPAlbuminPT 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 NN / slight elevate Elevate >4 times GGT,5’N NN

38 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

39 Manifestations of Liver Cirrhosis Fig. 42-5

40 40 S I R O S I S H A T I COMPENSATED PHASE : - Gangguan fungsi minimal ACTIVE PHASE : - Nekrosis progresif ( ALT  ) - Fibrosis  kolestasis ( ALP , BILI  ) DECOMPENSATED PHASE : - Gangguan fungsi berat + hipo albumin + hiperbilirubinemia  GAGAL HATI

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42 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/uL PLT /uL ALT 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 (+)

43 a.Apa diagnosis pasien ini? b.Ikterus tipe apa yang dialami oleh pasien sehingga terjadi peningkatan bilirubin?

44 Need a break?? 44


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