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Cholesterol and Lipids (*Cholesterol cholesterol important for the cell…

- - - - Notes:
        
        statins have 2 S/E
        --> myalgia
        --> hepatotoxicity
        
        fibrates and statins are contraindicated for myalgias
        --> Fibrates Vibrates the muscles
        
        ezetimibe and statins are contraindicated due to hepatotoxicity
        
        *Natural VLDL lowering agents = NFFL
        
        Niacin
        
        Fish Oil
        --> most have 2 main effects
        --> they both inhibit gallstone formation also
        
        Excercise/weight loss
        --> lower TAGs mainly
        --> minor = increase HDL and down LDLs
        
        *Fish Oil Omega 3
        
        changes the composition of cholesterol synthesis in the GB
        
        decreases cholesterol saturation in bile
        
        increase GB motility
        
        *Niacin
        
        "NICE Heavy DOUBBLE Ds"
        --> Niacin increases HDL
        
        Niacin also lowers VLDLs and thus FFAs
        
        Case examples
        
        Tetralogy case
        
        Notes:
        
        note that
        
        Clinical Case
        
        Fibrates
        
        Fibrate main action = increase Lipoprotein lipase
        --> increases the releasing of lipids from LDLs and Chylomicrons
        --> stores FFAs and lipids to remove them from the blood and causing damage
        
        secondary Fibrate action = inhibits cholesterol - hydroxylase enzyme
        --> lowers bile acid production
        
        fibrates are perfect storm for cholesterol gall stones
        --> increases FFAs and lipid storage (including cholesterol in t he GB)
        --> decreases the bile salts production (chol hydroxylase) that are needed to trap the cholesterol in micelles in the GB
        
        MOA
        
        Fibrates (eg, gemfibrozil, fenofibrate) activate peroxisome proliferator-activated receptor alpha (PPAR-α), which leads to decreased hepatic VLDL production and increased LPL activity.
        
        note this only works because you are raising the LPL = lipoprotein lipase and lowering the VLDL levels
        
        this way you stop VLDL bring cholesterol and FAs to periphery and allow HDLs to bring more to the liver with extra LPL activity to drop it off
        
        Fibrates Increase Cholesterol Gall Stones
        
        Fibrate main action = increase Lipoprotein lipase
        --> increases the releasing of lipids from LDLs and Chylomicrons
        --> stores FFAs and lipids to remove them from the blood and causing damage
        
        secondary Fibrate action = inhibits cholesterol - hydroxylase enzyme
        --> lowers bile acid production
        
        fibrates are perfect storm for cholesterol gall stones
        --> increases FFAs and lipid storage (including cholesterol in t he GB)
        --> decreases the bile salts production (chol hydroxylase) that are needed to trap the cholesterol in micelles in the GB
        
        1 more item...
        
        Statins = HMG-CoA reducatse Inhibitors
        
        HMG-CoA reductase inhibitors (+ secondary effects)
        
        rosuvastatin
        
        metabolized in the liver by CYP 3A4
        --> exception is pravastatin
        
        pravastatin (ONLY non- CYP 3A4 statin)
        --> dePRAVed of 3A4 metabolism
        
        atorvastatin
        
        Case examples
        
        Clinical Case
        
        Clinical Case
        
        Notes:
        
        note that
        
        Statin case
        
        Notes:
        
        note that
        
        Clinical Case
        
        statin with CYP enzymes interaction case
        
        Notes:
        
        note that
        
        Clinical Case
        
        Indications
        
        note that you should ALWAYS start someone on statins first line who have MI / CVA or CVD risk for MI
        
        most important thing to lower MI / CVA risks above everything else is lowering LDLs
        --> more than triglycerides or HDLs
        
        increased LDL receptors and LDL uptake
        
        secondary protection from statins
        
        Prescribing Statins:
        
        2 things to check before ever starting someone on statins
        
        check LFTs to make sure they won't cause hepatotoxicity
        
        check their other medications and screen for CYP inhibitors
        --> especially CYP 3A4 inhibitors, which metabolizes statins
        --> exception for CYP 3A4 is pravastatin that is dePRAVED of CYP
        
        Side Effects
        
        Hepatotoxicity
        --> need to check LFTs before starting anyone on statins
        
        Muscle toxicity = myalgia
        
        *Orlistat
        
        intestinal lipase inhibibitor
        --> this is a special drug of its own
        --> used to treat obesity that cannot be lowered by diet and exercise
        
        "Get ORLA THIN STAT!"
    - - *Lipoproteins
        
        LDL = Bad
        
        HDL = Nice
        
        *LDLs
        
        LDL = Bad
        
        HDL = Nice
        
        *Familial hypercholesteremia
        
        autosomal recessive and auto dominant
        
        decrease in liver LDL receptors
        --> can't bring Cholesterol back tot he liver
        
        get early onset atherosclerosis
        
        *HDLs
        
        LDL = Bad
        
        HDL = Nice
        
        *Apiloproteins
- - - - GnRH --> gonads
- - - - Type 1 Dyslipidemia
        
        auto recessive
        
        Deficient:
        
        TAGs
        
        Accumulation of:
        
        blank
        
        Presentation
        
        pancreatitis
        
        Type 2 A Dyslipidemia
        
        auto DOMINANT
        
        Deficient:
        
        LDL receptors
        
        Accumulation of:
        
        LDL (+ cholesterol)
        
        Presentation
        
        2 achillies tendons xanthomas
        
        2 eyeball senilis corneal arcus
        
        Type 2 B Dyslipidemia
        
        auto DOMINANT
        
        Deficient:
        
        blank
        
        Accumulation of:
        
        add VLDL onto type 2A
        
        Presentation
        
        same as Type 2 A
        
        Type 3 Dyslipidemia
        
        auto RECESSIVE
        
        Deficient:
        
        ApoE
        
        Accumulation of:
        
        Chylos and VLDLs
        
        Presentation
        
        Xanthomas on 3 fingers and palms
        
        Type 4 Dyslipidemia
        
        auto DOMINANT
        
        Deficient:
        
        ADDED VLDL chain production
        
        Accumulation of:
        
        VLDL + TAGs
        
        Presentation
        
        pancreatitis
        
        Type 5 Dyslipidemia
        
        auto
        
        A BETA APILOPROTEINEMIA - Dyslipidemia
        
        auto ?
        
        Deficient:
        
        BOTH major Beta apilo proteins = B100 and B48
        
        Accumulation of:
        
        NO lipid absorption/transport
        
        Presentation
        
        NO lipid absorption/transport
        
        most symptoms come from Vit E not absorbing
        
        acanthocyte = CANTHO = SPIKY RBCs
        --> gives a huge clue to this disease