RISIKO PJK
BY: WINANGUN.
PENDAHULUAN
DYSLIPIDEMIA MASALAH KESEHATAN,
PENYAKIT DEGENERATIF ↑↑, GERIATRI,
ATEROSKLEROSIS, PJK, STROKE. 80% F
DAN >> KEMATIAN PADA DM.75%
LIPID PENTING UNTUK: MEMBENTUK DAN
FUNGSI SEL, SUMBER ENERGI, PELINDUNG
TUBUH, SYNTESE HORMON STEROID,
PERKURSOR PROSTAGLANDIN,
LIPID TAK LARUT AIR IKAT APOPROTEIN
LIPOPROTEIN LARUT AIR SIRKULASI
LIPOROTEIN ADA 5: KILOMIKRON, VLDL. IDL,
HDL DAN LDL YANG PALING JAHAT.
PENGERTIAN
DYSLIPIDEMIA: KELAINAN METABOLISME
LEMAK TUBUH DITANDAI ↑↑ ATAU ↓ FRAKSI
LIPID DL PLASMA. ↑KOLESTEROL TOTAL, TG
DAN LDL SERTA ↓↓ HDL.
KOMPONEN PENTING ATEROSKLEROSIS
DIKENAL TRIAD LIPID.
KECENDRUNGAN ↑↑ KASUS DYSLIPIDEMIA
GG VASKULER , ATEROSKLEROSIS PJK ,
STROKE PERLU PENCEGAHAN & TH/
MENYELURUH.
KOLESTEROL
dalam jumlah tepat bermanfaat, Jika berlebih berbahaya
MANFAAT KOLESTEROL
Sumber energi
Pembentukan dinding sel
Pembentukan hormon
Kolesterol Total
Trigliserida
Kolesterol-LDL
Kolesterol-HDL
Kolesterol dari makanan Kolesterol tidak dapat larut
dalam air (darah)
Agar dapat diangkut ke sel
Diolah dalam saluran cerna
yang memerlukan, kolesterol
berikatan dengan protein
membentuk Lipoprotein
Diserap masuk aliran darah
Contoh Lipoprotein :
Kilomikron
HDL (High Density Lipoprotein)
Didistribusikan ke sel-sel LDL (Low Density Lipoprotein)
Yang memerlukan
KLASIFIKASI
A.KAUSA:
1. DYSLP. PRIMER >> FAKTOR GENETIK
2. DYSLP. SKUNDER: E/ PENYAKIT TT:
HYPOTYROID, DM, NS, SH, CRF DLL DAN
OBAT2AN: DIURETIK, β BLOKER, ESTROGEN
B. KLINIS:
1.HYPERKOLESTEROLEMIA, ( HYPERKOLEST)
2.HYPERTRIGLISERIDEMIA,( HYPER TG)
3.CAMPURAN
KRETERIA DIAGNOSTIK
PATOKAN NILAI KOLESTEROL DIKAITKAN DG
RISIKO PJK ≈ Penelitian jangka panjang
a. KADAR MASIH AMAN << 200 mg/dl
b. KADAR BORDRLINE HIGH: 200-239 mg/dl
c. KADAR TINGGI BERBAHAYA >> 240 mg/dl.
KESETARAAN KOLESTEROL TOTAL DG LDL.
KOL: 240 mg/dl LDL 160 mg /dl
KOL: 200 mg/dl LDL 130 mg/dl
KOL: 155 mg/dl LDL 100 mg/dl
HUBUNGAN PROFIL LIPID
DG RISIKO PJK
KADAR DESIRE BORDER HIGH
KOLES ABLE LINE
TOTAL << 200 200-239 >> 240
KO LDL
PJK (-) << 130 130-159 >> 160
PJK (+) << 100 - -
HDL >> 45 35-45 << 35
TRIGLI
PJK (-) << 200 200-299 >> 400
Fredrickson Classification of Hyperlipidemias
multiple major risk factors (especially diabetes); severe and poorly controlled risk factors (eg, cigarette smoking); metabolic
syndrome (triglycerides [TG] ≥200 mg/dL + non–HDL-C ≥130 mg/dL with HDL-C <40 mg/dL); and acute coronary
syndromes.1
1. Grundy SM et al. Circulation. 2004;110:227–239.
2. Smith SC Jr et al. Circulation, 2006; 113:2363–2372.
Many High-Risk Patients Were Not Tested and Many Who
Were Tested and Treated Did Not Achieve
LDL-C 100 mg/dL1
In a retrospective subgroup analysis of patients with CHD (N=3,320), only 42.7% received lipid testing (n=1,418) within 6
months of diagnosis. Of the 1,418 CHD patients who were tested, 70% had an LDL-C ≥100 mg/dL.
At 6 months At 12 months
Treatment defined as 1 or more prescription fills within a 6-month period (mean days supply = 150) for CHD patients.
Of those who did not achieve LDL-C <100 mg/dL at 6 months and continued treatment, 51.9% (n=122) attained LDL-C <100 mg/dL within the
entire follow-up period (average 25 months).1
In 1999, ATP II recommended an LDL-C goal of ≤100 mg/dL for patients with CHD.2
1. Data available on request from Merck & Co., Inc., Professional Services-DAP, WP1-27, PO Box 4, West Point, PA 19486-0004. Please specify information
package 20507201(1)-MSP.
2. The Expert Panel. Summary of the Second Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and
Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). JAMA. 1993; 269; 3015–3023.
Dual Inhibition of Cholesterol
Synthesis and Absorption
Diet
Liver
Bile
Bile acids Statin
Ezetimibe
Excretion in Atherogenic
feces lipoproteins
Atherosclerosis Timeline
Foam Fatty Intermediate Fibrous Complicated
Cells Streak Lesion Atheroma Plaque Lesion/Rupture
Endothelial Dysfunction
From first decade From third decade From fourth decade
Smooth muscle Thrombosis,
Growth mainly by lipid accumulation and collagen hematoma
Dapat dimodifikasi :
• Lipid/lemak dan Lipoprotein
• Diabetes Melitus
• Hipertensi
• Kebiasaan Merokok
• Obesitas (kegemukan)
E Hubungan
R Lemak
A
T PJK
LEMAK
Kolesterol
Trigliserida
Fosfolipid
Asam Lemak
Kilomikron
Mengangkut lemak dari saluran cerna menuju hati
LDL – teroksidasi 1
paling berbahaya
LDL – densitas kecil 2
lebih berbahaya
LDL – kolesterol 3
berbahaya
KOLESTEROL
fosfolipid
Kolesterol
bebas
apolipoprotein
Lipoprotein
Kilomikron Mengangkut lemak menuju hati
ApoE mediated
Kolesterol HDL
Pembersih Kolesterol kolesterol
baik
Apoprotein A-1
Komponen utama HDL
Pembersih lemak
Apoprotein B
Komponen utama LDL
LDL KOLESTEROL
LDL – teroksidasi 1
paling berbahaya
LDL – densitas kecil 2
lebih berbahaya
LDL – kolesterol
berbahaya 3
KOLESTEROL–LDL (Direk)
KEUNGGULAN
n = 4797
Triglyceride levels
1. Lebih Akurat
Kemungkinan kesalahan perhitungan 201-300 mg/dL (2.27-3.39 mmol/L): 23%
Diperkirakan dari
LDL-Kolesterol/Apo B < 1,2
LDL kecil padat (SMALL DENSE LDL)
LEBIH BERBAHAYA
KARENA :
• Mudah terperangkap dan masuk ke dalam
lapisan dinding pembuluh darah (Intima)
karena ukurannya lebih kecil
• Mudah teroksidasi menjadi Oxidized-LDL
OXIDIZED – LDL
LDL YANG PALING BERBAHAYA
KARENA :
SERANGAN JANTUNG/STROKE
Oksidasi LDL
MENGAPA BERBAHAYA
(dianggap sebagai Faktor Risiko) ?
Hipertrigliseridemia
Lack of Interest
The
Solution…
Engage the
Patient
B. PENGOBATAN
1. TH/ NON FARMAKOLOGIK:
a.PENYULUHAN
b.PERENCANAAN MAKAN / DIET,
c. LATIHAN JASMANI / OLAH RAGA TERATUR,
d. PENGENDALIAN GULA DARAH PD DM
2. TH/ FARMAKOLOGIK / OBAT HYPOLIPIDEMIK
a. PENGIKAT RESIN: KOLESTIPOL, KOLESTIRAMIN
b. ASAM NIKOTINAT: ACIPIMOX, ASAM NIKOTINAT
c. GOLONGAN FIBRAT: GEMPIBROSIL, FENOFIBRAT
d. GOLONGAN STATIN: SIMVASTATIN,LOVASTATIN,
ATORVASTATIN, FLUVASTATIN. DLL.
Mechanism of
Intestinal-Acting Agents
Intrinsic
Motivation
Manfaat pemantauan glukosa
darah mandiri
Penyesuain diet
vs