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optimal ldl cholesterol
<100 mg/dl
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optimal total cholesterol
<200mg/dl
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optimal HDL cholesterol
> 60 mg/dl
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optimal triglyerides
<150 mg/dl
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Bile Acid Sequestrants
Cholestyramine granules, colestipol, colesevelam
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mechanism of action of bile acid sequestrants
binds bile acids in the liver which disrupts the recirculation stimulates the live to break down the cholesterol to bile acids, increase the update of LDL and then reduce the LDL concentration
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Are bile acid sequestrants systemically absorbed
NO
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What are side effects of Bile Acid Sequestrants
GI problems and a small tranient low percentage of patients saw an increase in triglycerides
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what are drug interactions wtih bile acid sequestrants
they bind to other drugs and vitamens so patients need to take the medication at a seperate time from other medications
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bile acid sequestrants works on what type of cholesterol
LDL only!
it does not raise HGL or significantly change TG
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HMG-coA reductase inhibitors
- statins
- atorvastin, fluvavastin, pravastatin, simvastatin, rosuvastatin, pitavastatin
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how to HMG CoA reducatase inhibitors work
HMG-CoA reductase is the enzyme that is responsible for voncerting HMG-CoA to mevalonate which is the early rate limiting step in cholesterol synthesis.
it works at the first rate limiting step to lower the production of cholesterol. works like a bottle neck, stop the production from the top
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what time of day should HMG-CoA reducatse inhibitors be taken at and why?
should be taken at night because thats when the body produces most of the cholesterol
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side effects of HMG-CoA reducatse inhibitors
increased LFTs and myopathy/myalagia/myositis/rhabdomyolysis (muscle aches and pains)
the higher the dose the most likely that you are to experience the side effects
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drugs that cause muslcle aches
niacin and HMG-CoA reducatse inhibitors
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mechanism of action of muscle aches
generally unknown but believed to be a ubiquinone deficiency where the ubiquinone is replaced by coenzyme coq10
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myopathy
general term related to any muscle complaint
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myalgia
muscle complaints without elevation in creatine kinase
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myositis
- muscle complaints with elevtion of creatine kinase
- this is more severe because there is muscle inflammation
- creatine kinase breaking down is a possible proble problem if it causes liver damage and breakdown
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rhabdomyolysis
elevated levels of creatine kinase which are greater than ten times the upper limits of normal. also brown urine and urinary myoglobin-looks like there is blood in the urine
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statin interactions
grapefruit juice-it inhibits the metabolism of the statin, thus more of it is left in the system than is supposed to. this can leave to overdosing as well as muscle achines and pains, breakdown adn renal failure
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nicitinic acid mechanism of action
reduces the production of VLDL in the liver- decreases the snthesis of LDL as well as decreases tri glycerides and increases HDL. it works by decreasing cholesterol biotransformation in the liver
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nicotinic acid dosing
start by titrating a dose of immediate release adn then working up to sustained release. sustained release medications have a more likely side effect, such as hepatotoxicity however it is easier for the patient to take the medication once a day versus several times
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side effects of nicotinic acid
cutaneous flushing for the skin from the neck up (cosmetically only), pruritis and liver dysfunction
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fibric acid derivitives
gemfibrozil, fenofibrate, fenofibric acid
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fibric acid mechanism of action
lowers triglycerides only
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side efects of fibric acid derivitives
gall stones and cholecystitis
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