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Transcript of PATOLEMAK3
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Pemeriksaan LaboratoriumGangguan Metabolisme Lemak /
Dislipidemia
JUSAK NUGRAHA2010
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Prasyarat Kuliah
• Telah menguasai dasar2 Biokimia & FaalLemak dalam tubuh manusia
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GANGGUAN METABOLISME LEMAK
• HIPERLIPOPROTEINEMIA = Lipoprotein• HIPERLIPIDEMIA = Fraksi lipid • HIPERLIPEMIA à kekeruhan serum (lipemik)• HIPOLIPOPROTEINEMIA / ALIPOPROTEINEMIA• SEKARANG à DISLIPIDEMIA:
ABNORMALITAS FRAKSI LIPID DALAM SERUM
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LEMAK DARAH• MENGAPA Mempelajari lemak darah?à PATOGENESIS ATEROSKLEROSIS (penyebabmortalitas & morbiditas terpenting)
1. PJK 2. Stroke • FAKTOR RESIKO:
- GENETIK - OBESITAS - DISLIPIDEMIA - INAKTIVITAS FISIK- DM - STRES MENTAL- HIPERTENSI - KEPRIBADIAN TIPE A - MEROKOK (RESPONSIF BERLEBIHAN)
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KULIAH PRASYARAT
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Familial Combined Hyperlipidemia
The most common familial cause of elevated LDL The most common familial cause of elevated LDL cholesterol is known as familial combined cholesterol is known as familial combined hyperlipidemiahyperlipidemia, found in about 15% of patients , found in about 15% of patients with premature CHD . These patients have been with premature CHD . These patients have been shown to have increased production of veryshown to have increased production of very--lowlow--density lipoprotein (VLDL) density lipoprotein (VLDL) apolipoproteinapolipoprotein ((apoapo) ) BB--100. Affected family members have elevated 100. Affected family members have elevated triglyceride levels, elevated LDL cholesterol triglyceride levels, elevated LDL cholesterol levels, or both. Moreover, affected family levels, or both. Moreover, affected family members often have low HDL cholesterol. The members often have low HDL cholesterol. The final steps in the cholesterol synthesis pathway final steps in the cholesterol synthesis pathway are shown in Fig. 2. Here are shown in Fig. 2. Here squalenesqualene is converted is converted into into lanosterollanosterol
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Tahap akhir sintesis kolesterol
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PATOKIMIAWI LEMAK1. MEMAHAMI BATASAN LEMAK 2. MEMAHAMI MACAM LEMAK & SISTIM
TRANSPORTASINYA DALAM DARAH3. MEMAHAMI BEBERAPA GANGGUAN
METABOLISME LEMAK4. MENGETAHUI PRINSIP PEMERIKSAAN
LABORATORIUM DARI LEMAK DARAH & CARA INTERPRETASINYA.
LEMAK (LIPID): SENYAWA YG SECARA LANGSUNG/TIDAK LANGSUNG BERHUBUNGAN DENGAN ASAM LEMAK
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LEMAK DARAH (LIPID)• LIPID dalam darah berupa:
- KOLESTEROL (20%)- TRIGLISERIDA (30%)- FOSFOLIPID (45%)- ASAM LEMAK- LEMAK LAIN DALAM JUMLAH KECIL
DAN TAK PUNYA ARTI PENTING• LIPID ini berasal dari:
1. MAKANAN: absorbsi usus2. SINTESIS ENDOGEN: biosintesis dari kabohidrat danprotein
LIPID: sumber energi yang besar & water-insoluble à perlusistim transportasi khusus
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LIPOPROTEIN• Lipid + Apoproteinà kompleks makromolekul
yang water-soluble• 4 lipoprotein utama: kilomikron, VLDL, LDL, HDL• 2 lipoprotein khusus: Lp (a) , LpX• Bentuk antara: IDL• Lipoprotein dapat dipisahkan dengan:
Ultrasentrifus: berdasarkan densitasElektroforesis: berdasarkan muatan apo-prot
- +β
ki β Pre-β a
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APOPROTEIN (APO-LIPOPROTEIN)• ADALAH FRAKSI PROTEIN PADA LIPOPROTEIN• APOPROTEIN – AI / AII / AIV• APOPROTEIN – B48 / B100• APOPROTEIN – CI / C II / CIII• APOPROTEIN – E • APOPROTEIN – a (Apo-a)
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• • ApoA-I: principal structural protein of HDL but also found in chylomicrons and activates lecithin:cholesterol acyltransferase (LCAT).
• • ApoA-II: another structural protein of HDL also found in chylomicrons and activates hepatic lipase (HL).
• • ApoA-IV: predominantly found in HDL and activates LCAT and lipoprotein lipase (LPL).• • ApoB-48: exclusively found in chylomicrons, derived from the apoB-100 gene, and reduced
to 48% of the N-terminal component of B-100 by RNA editing, with no LDL receptor (LDLr) binding domain.
• • ApoD: exclusively found in HDL and possibly activates CE transfer protein (CETP) (2).• • ApoE: also found broadly in HDL, IDL, LDL, VLDL, and chylomicrons and binds to• LDLr with varying affinity dependent on the inherited apoE allele. Three different apoE• isoforms exist in humans: apoE2 with lower affinity to LDLr, apoE3 with intermediate• binding affinity, and apoE4 with higher affinity (3).• • Apo(a): distinguishing structural protein of Lp(a) that is covalently bound to apoB-100and inhibits plasminogen activation (4,5).
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• ApoB-100: principal structural protein of LDL, alsofound in VLDL, IDL, and Lp(a); ligand for LDLr.
• ApoC-I: primarily found in HDL and chylomicronsand also in IDL and VLDL and
activates LCAT.• ApoC-II: protein primarily of VLDL and chylomicrons
and also found in HDL and IDLand activates LPL.• ApoC-III: found broadly in HDL, IDL, LDL, VLDL, and
chylomicrons but more consistentlyin VLDL and chylomicrons and inhibits LPL .
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• ApoD: exclusively found in HDL and possibly activates CE transfer protein (CETP) .
• ApoE: also found broadly in HDL, IDL, LDL, VLDL, and chylomicrons and binds to LDLr with varying affinity dependent on the inherited apoE allele. Three different apoE isoforms exist in humans: apoE2 with lower affinity to LDLr, apoE3 with intermediate binding affinity, and apoE4 with higher affinity .
• Apo(a): distinguishing structural protein of Lp(a) that is covalently bound to apoB-100 and inhibits plasminogen activation
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apoprotein
Fosfolipid
Kolesterolbebas
Kolesterolester
Trigliserida
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KILOMIKRON
• d < 0,94• Mobilitas elektroforesis: origin• Kaya akan TG exogen, à absorbsi lemak oleh
usus• Hanya ada di darah post prandial• Fungsi: transpost lipid exogen
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VLDL (Pre ß Lipoprotein)• d = 0,96-1,006. • Mobilitas elektroforesis: pre-Beta• Mengangkut TG & lemak lain yang disintesis di
hati• Fungsi: mengangkut lipid ke jaringan perifer
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LDL (ß-Lipoprotein)• d = 1,006 – 1.063• Kaya akan kolesterol &
Dibentuk di plasma, berasal dari degradasi VLDL.
• Fungsi: mengangkut kolesterol ke jaringan perifer.
• Apoprotein: B100, B48
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HDL (α-Lipoprotein)
• d = 1,063 – 1,21• Kandungan protein tinggi (Apo A,C,E, tu A1)• Fungsi: mengambil kolesterol dari jaringan perifer ke
hati, lalu didegradasi atau diekskresi empedu (removal / reverse transport dari kolesterol)
• Dari degradasi VLDL & kilomikron. Inti HDL = kolesterol ester yang diambil di jaringan perifer dengan bantuan enzim LCAT.
• Faktor protektif
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Beberapa reaksi yang penting• LIPOLISIS : penguraian Trigliserida menjadi
asam lemak bebas dan gliserol oleh enzim LPL – Lipoprotein Lipase
• Esterifikasi kolesterol : oleh enzim LCAT = Lecithin Cholesterol- acyltransferase
• Sintesis Kolesterol intraseluler: oleh enzim HMG-CoA reduktase
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Metabolic Map of Lipoproteins
Chylomicron CMremnant
Liver
Intestine
Capillary endothelial cellsUnesterified cholesterol
Receptor
Peripheral cell
Bloodstream
LPL: lipoprotein lipase
HTGL: Hepatic triglyceride lipoprotein
LCAT: Lethitin cholesterol acyltransferase
VLDL I DL LDL
I, V IIb, IV, V III IIa, IIb
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TEORI TERJADINYA ATEROSKLEROSIS
1. HIPOTESIS INFILTRASI LIPID: infiltrasi lipoprotein ke intima
2. Hipotesis Kerusakan Endotel: trombogenesis & PDGF
3. TEORI RESEPTOR & RADIKAL BEBAS
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Small dense (sd)-LDL
• Sd-LDL: mudah teroksidasià : peran pentingaterogenesis.
• Tak dikenali oleh reseptor LDL• Di”makan” melalui scavenger receptor macrophage. • Merangsang endotel mengeluarkan MCP-1
(Monocyte-chemotactic protein) & M-CSF (Macrophage-colony stimulating factor)
• Migrasi monosit ke endotel• Ferritin: besi bebasà peran penting oksidasi LDL
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DISLIPIDEMIA
• DISLIPIDEMIA PRIMER : FAKTOR GENETIK• DISLIPIDEMIA SEKUNDER :
‘’GAYA HIDUP” & DASAR PENYAKIT LAIN
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Batas normal Lipid (NCEP-ATP III)
• Kolesterol total : < 200 mg/dl• Kolesterol-HDL : > 45 mg/dl• Kolesterol-LDL : < 100 mg/dl• Trigliserida : < 150 mg/dl• Rasio Kolesterol total/HDL : < 5
• Kolesterol LDL:– Asai laboratorik, pengendapan polianion– Perhitungan Formula Friedewald
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Pemeriksaan Laboratorium dasar• Pengamatan plasma/ serum segar: apakah
keruh seperti susu = lipemik.• Tes kilomikron (Plasma standing test)• Kadar Kolesterol (total)• Kadar Trigliserida• Pengendapan dengan poli-anion bervalensi
dua : heparin-Mn.HDL ètdpt pd supernatanLDL à tdpt pd bagian endapan
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TES KILOMIKRON (PLASMA STANDING TEST)TES KILOMIKRON (PLASMA STANDING TEST)
•• SERUM/PLASMA DALAM TABUNG DIDIAMKAN SERUM/PLASMA DALAM TABUNG DIDIAMKAN SEMALAM PADA SUHU 4SEMALAM PADA SUHU 400CC
NN I IIA IIB III IV V
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Formula Friedewald
• Kol-LDL = Kol Total – (Kol-HDL) – TG/5• Berlaku untuk serum/plasma puasa
(kilomikron = 0 )• Syarat: TG < 400 mg/dl (Kol-VLDL≠TG/5)
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KLASIFIKASI HIPERLIPOPROTEINEMIA MENURUT FREDRICKSON
TIPETIPE KELAINAN LIPOPROTEINKELAINAN LIPOPROTEIN
II Lapisan kilomikron di atas plasma puasaLapisan kilomikron di atas plasma puasa
IIaIIa KenaikanKenaikan LDLLDL
IIbIIb Kenaikan LDL , disertai VLDLKenaikan LDL , disertai VLDL
IIIIII Terdapat bentuk Intermediate (Terdapat bentuk Intermediate (floating ß floating ß ))
kilomikron mungkin meningkatkilomikron mungkin meningkat
IVIV Kenaikan VLDL sajaKenaikan VLDL saja
VV KenaikanKenaikan kilomikronkilomikron & VLDL & VLDL padapada plasma plasma puasapuasa
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TIPE 1 (Hiperkilomikronemia)
• Etiologi: Primer – GENETIK.Def LipoProteinLipaseSekunder: SLE
Dis-γ-Globulinemia
Insulinopenic DM
• Resiko aterosklerosis: rendah
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DISLIPIDEMIA SEKUNDER
HIPERKOLESTEROLEMIA HIPOTIROIDSINDROMA NEFROTIKDIS-GAMMAGLOBINEMIAPORPHYRIAPENYAKIT HATI
HIPERTRIGLISERIDEMIADIABETES MELLITUSOBESITASALKOHOLISMEPANKREATITISGAGAL GINJAL KRONISDIS-GAMMAGLOBULINEMIAGLIKOGEN STORAGE DISEASE
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Pengukuran Apoprotein• Pengukuran Apo A1 àmewakili HDL• Pengukuran Apo B (apo B100) àmewakili LDL +
(VLDL)• Pengukuran Apo A1 & Apo B à Lebih baik
daripada Kolesterol-HDL &-LDL untuk menentukanresiko hiperlipidemia.
• Apo A1 & B àDiperiksa bila Kolesterol HDL / LDL = abN atau ada faktor resiko + dislipidemia
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Penanggulangan gangguan metabolismelemak
• Pengaturan “gaya hidup” : diet, BB, olahraga• Pengobatan farmakologis:
1. Sequestran asam empedu2. Asam nikotinat3. Golongan Fibrat4. Golongan Statin (HMG-CoA reductase inhibitor)
• Pembedahan
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Lp (a)• Autosomal dominant• > 30 mg/dl à resiko PJK 2X• Faktor resiko sendiri, tak berhub. Dg fraksi lemak
lain• Struktur mirip LDL, tapi punya “ekor” apo(a) &
apoB100• Struktur Apo(a) mirip plasminogen à
menghambat kerja plasminogen à Plasmin tak terbentuk à tak terjadi Fibrinolisis .
• Jadi punya efek TROMBOGENIK
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Sifat2 Lp(a)
• Bergerak pada pre-ß elektroforesis• Struktur mirip LDL• Ukuran LDL < Lp(a) < VLDL• Mempunyai bagian protease serine yang mirip
plasminogen
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Peran Lp(a) pada aterosklerosis1. Lp(a) berikatan dgn reseptor plasminogen
(kompetitif) yg tdpt pd trombosit, endotel, fibroblast. Sehingga konsentrasi Lp(a) yg >> à aktivitas antifibrinolisis
2. Penimbunan Lp(a) pada endotel arteri, ikatan lp(a) dengan makrofag arteri
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Hubungan TG & atherosklerosis
• Dahulu: TG bukan faktor resiko PJK, melainkan resiko pankreatitis akuta
• Sekarang: terbukti TG mempunyai peran penting pada Atherosklerosis. Peran TG:
1. TG mengganggu transpor oksigen ke jaringan2. TG memacu agregasi trombosit3. TG merangsang terbentuknya mikrotrombus4. TG menurunkan kadar HDL
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•Metabolic syndrome (MetS) is a dyslipidemic state that is associated with a cluster of risk factors.
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Metabolism of Triglyceride
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> 3 Kriteria (IDF 2005)
• Obesitas sentral ( lingkar perut > 90 cm (L), > 80 cm (P)
• Trigliserida ( > 150 mg/dl)• HDL-C ( < 40 mg/dl (L); < 50 (P)• Blood Pressure (> 130/85 mmHg)• Glukosa puasa ( > 100 mg/dl)
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Parameter Evaluasi
1. Atherogenic Dyslipidemian Elevated fasting TGn Elevated Apo Bn Elevated remnant Lipoproteinemian Increased sd-LDL : LDL/ApoB < 1,2
2. Insulin Resistancen Hyperinsulinemia, Hyperglycaemia
3. Prothrombotic State / Proinflammatory Staten Fibrinogenn Adiponectinn hs-CRP
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Penyebab Hipertrigliseridemia Primer
• Familial combined hyperlipidemia• Familial Hypertriglyceridemia• Type III Hyperlipoproteinemia• Chylomicronemia:
– Lipoprotein lipase deficiency– Apolipoprotein C-II deficiency
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Penyebab Hipertrigliseridemia Sekunder
• Resistensi Insulin– Diabetes Mellitus (DM)– Metabolic Syndrome
• Alkohol• Excess Carbohydrate intake• Nephrotic syndrome• Hypothyroidism• Medications: Beta-blockers, immunosupressive
drugs, protease inhibitor, estrogen replacement, isotretinoin.
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Uji Laboratorium untuk Pengelolaan Penyakit Kardiovaskular
Faktor risiko Petanda baru Penyakit Arteri Koroner
Petanda Infeksi /
Inflamasi –– Total Cholesterol– HDL-Chol– LDL-Chol– Apolipoprotein A-I– Apolipoprotein B– Lp (a)– Triglyceride– CRP– SAA– Fibrin D-Dimer– Factor VII– von Willebrand Factor– Plasminogen Activator I– Fibrinogen
– Homocystein– etc.
Øsd-LDLØMyeloperoxidase(MPO)
Ø ox-LDLØF2Isoprostane
ØSphingomyelinase
Ø Phospholipase A2
family (Lp-PLA2; sPLA2)
Ø hsCRP
–Helicobacter pylori
– Chlamydia
– Cytomegalovirus
– CRP
– SAA
MS
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PARAMETER LAIN RESIKO ATEROSKLEROSIS
• Fibrinogen & faktor VII• ACA (anti Cardiolipin antibodies)• Ferritin• Homocysteine• Hs-CRP