hypolipidemic pharmacology outline
TRANSCRIPT
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HYPOLIPIDEMIC DRUGS
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EZETIMIBE
1. IN FOOD WE CONSUME CHOLESTEROL AND TG
2. IT IS ABSORBED IN INTESTINE, TAKEN BY LACTEALS
3. FROM LACTEALS CHOLESTEROL AND TG TAKEN THROUGH THORACIC DUCT TO BLOOD VESSEL WITH HELP OF CHYLOMICRONS
4. IN BLOOD VESSEL ,
LIPO PROTEIN LIPASE
TG FATTY ACID + GLYCEROL
FATTY ACID TAKEN UP BY ADIPOSE CELLS AND GETS CONVERTED TO TG AGAIN
FIBRATES
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5. REMANANT CHYLOMICRON ENTERS THE LIVER
6. LIVER SECRETE TG AND CHOLESTEROL INTO BLOOD VESSEL AS VLDL
7. THIS TG AGAIN GETS METABOLISED IN BLOOD VESSEL BY LPL
8. THUS NOW VLDL NOW CHANGES TO IDL
TAKEN BACK TO LIVER
IDL CONVERSION TO LDL CONTAINING ONLY CHOLESTEROL AND DISTRIBUTED TO VARIOUS TISSUE
LPL
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9. HDL CARRIES CHOLESTEROL FROM PERIPHERY TO LIVER
10.CHOLESTEROL IS EXCRETED IN BILE IN FREE FORM AND AS BILE SALTS
11.BILE SALTS UNDERGO ENTEROHEPATIC CIRCULATION BILE ACID
BINDING RESINS
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• STATINS – INHIBIT HMG CO-A
• NIACIN – INHIBIT LIPOLYSIS IN ADIPOSE TISSUE .
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DRUGS
• STATINS ( LDL )
• BILE ACID BINDING RESINS
• INTESTINAL CHOLESTEROL ABSORPTION INHIBITORS - EZETIMIBE
• FIBRATES (TG)
• NIACIN (HDL)
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HYPER LIPOPROTEINEMIA
• PRIMARY
• SECONDARY
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TYPE 1 – FAMILIAL LIPOPROTEIN LIPASE DEFICIENCY
TYPE 2A – FAMILIAL HYPER- LDL
CHOLESTROLEMIA
TYPE 2B – FAMILIAL COMBINED- VLDL , LDL
HYPERLIPIDEMIA
TYPE 3 – FAMILIAL DYSBETA- MutationLIPOPROTEINEMIA
TYPE 4 –FAMILIAL VLDL
HYPERTRIGLYCERIDEMIA
TYPE 5 – FAMILIAL MIXED VLDL , CM
HYPERTRIGLYCERIDEMIA
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STATINS
• MECHANISM
• DRUGS – PRAVASTATIN , ATORVASTATIN
• PHARMACOKINETICS – ORALLY, M-LIVER ,
E- KIDNEY
• USES – PLEOTROPIC EFFECT , PRAVASTATIN FIBRINOGEN LEVEL
• A/E – HEPATOTOXITY , MYOPATHY AND RABDOMYOLYSIS ( PRAVASTATIN )
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BILE ACID BINDING RESINS
• MECHANISM
• DRUGS – CHOLESTYRAMINE , COLESTIPOL
• PHARMACOKINETICS – ORALLY , EXCRETED IN FAECES
• A/E- FLATULENCE AND CONSTIPATION
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INTESTINAL CHOLESTEROL ABSORPTION INHIBITOR
• MECHANISM
• DRUGS - EZETIMIBE
• PHARMACOKINETICS – ORALLY , EXCRETED IN BILE
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FIBRATES• MECHANISM
• DRUGS – GEMFIBROZIL , FENOFIBRATE
• PHARMACOKINETICS – ORALLY , M- LIVER , E –URINE
• USE –FIBRATES PLASMA FIBRINOGEN , HYPERURICEMIA
• A/E – MYOPATHY
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NIACIN
• MECHANISM
• PHARMACOKINETICS – ORALLY , M- LIVER ,E -URINE
• A/E – FLUSHING , HYPERURICEMIA , HEPATOTOXITY
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THANKYOU…..