By Asmaa badawy. Dyslipiderrnia.
Lipoproteins. Lipid Protein Lipoprotein.
Lipoprotein = lipid transport.
Causes of Hyperlipidemia Lifestyle Diabetes Mellitus Kidney disease Pregnancy Hypothyroidism Genetic Alcohol Dyslipidemia Drugs- Thiazides, Cyclosporin, Glucocorticoids, Beta Blockers..
Protein Phospholipid Cholesterol Triglyceride A. A lipoprotein 0000 0 Chylomicron — VI-DL HDL B. The variety Of lipoproteins Blood Lipids Serum Triglycerides • VLDL • CHYLOMICRONS Serum Cholesterol • LDL (Bad, 77.5%) • HDL (Good, 17.5%) IDL (Neutral, 5%).
1-chylomicron mainly T.G carry lipid from intestine to liver 2-VLDL mainly T.G from liver to blood 3-ILDL half cholesterol half T.G 4-LDL mainly cholesterol bad cholesterol 5-HDL from tissues to liver good cholesterol.
6/1/2022. Life Cycle of Cholesterol-carrying LIPOPROTEINS Liver produces LIPOPROTEINS LDL Lipoprotein Molecule Triglyceride (fat) VLDL fat ce Ils TRIGLYCERIDE Muscle burn TRIGLYCERIDE.
0.95 1 .006 1 .02 1 .06 1.10 1.20 HDL o 5 o 10 IDL LDL 20 VLDL 40 Diameter, nm Chylomicron remnants Chylomicron 60 80 1 ooo.
Antihyperlipedemic drugs. Hyperlipidemia SINGLE USE ONLY.
Classification. Statins Niacin Fibrates Bile acid resins, Ezetimibe.
BILE ACID-BINDING RESINS (CHOLESTYRAMINE) 1-Bind to bile acids in the intestine decrease cholesterol and T.G absorption 2-prevent their absorption and . preventing the recycling of bile acids, bile acid-binding resins divert hepatic cholesterol to synthesis of new bile acids, thereby reducing the amount of cholesterol..
Mechanism of action. ÙØªÙجة Ø¨ØØ« Ø§ÙØµÙر ع٠âªbile binnding resinâ¬â.
Side effect 1-GIT disturbance (steatorrhea) 2-decrease absorption of fat soluble vitamins 3-cholesterol gall stones.
EZETIMIBE.
Mechanism of action Selective inhibition of cholesterol absorption both 1-exogenous (dietary ) 2-endogenous (biliary).
Preparations (HMG CO A Reductase inhibitors) atorvastatin, simvastatin.
Mechanism of action Inhibition of HMG-co A reductase decrease so, inhibit synthesis of cholesterol in liver.
Side effects of statins MUSCLE Muscle pain Rhabdomyolysis LIVER Liver failure.
ÙØªÙجة Ø¨ØØ« Ø§ÙØµÙر ع٠âªniacin hypolipidemicâ¬â.
Mechanism of action ( agonist to nicotinic acid VIT B3 ) Inhibition of lipolysis decrease FFA production decrease T.G synthesis in liver.
S.E OF NIACIN 1-increase P.G vasodilators hypotension ,flushing(can be managed by NSAIDS ) 2- increase histamine release in GIT HCL secretion ,colic.
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Mechanism of action of fibrates Agonist of PPAR nuclear receptor (activation of lipoprotein lipase) metabolism of T.G.
26. 1- GIT disturbance 2-cholesterol gall stones 3-liver enzymes elevation 4-myopathy.
COMBINATION THERAPY: Drug combinations are often required to achieve the maxi- mum lowering effect with minimum toxicity Certain drug combinations provide advantages whereas others present specific challenges..
Because resins interfere with the absorption of certain HMG-CoA reductase inhibitors these must be given at least 1 h before or 4 h after the resins. The combination of reductase inhibitors (statin) with fibrates increases the risk of myopathy..
1-statin,resin (time interval) 2-statin ,niacin 3-niacin,resin Good combinations 1-fibrate,resin both increase gall stones 2-statin,fibrate both hepatotoxic ,myopathy Bad combinations.
ØµÙØ±Ø© ذات ØµÙØ©.