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name the fat soluble vitamins
describe action of bile acid sequestants
- they bind to bile acids (made of cholesterol) form large, insoluble complexes that can't be reabsorbed from small intestine to go back to liver, and are excreted instead.
- loss of these bile acids makes liver synthesis more bile acids --> cycle continues and cholesterol continues to be excreted
what cycle/circulation do bile acid sequestrants interrupt?
- normally bile is secreted by liver to emulsify fats in small intestine, then reabsorbed in ileum to return to liver and become part of bile; cholesterol in bile acids is recycled and only small amts leave body in feces.
how do bile acid sequestrants interact with lipid soluble drugs and vitamins?
they are not absorbed b/c bile acids are needed to break them down for absorption.
- -can lead to vitamin deficiencies of a, d, e, k
- -digoxin and coumadin: binds to these drugs and decreases their absorption
- -(book says coumadin can become increasingly effective, not less so, because of vit K deficiency)
bile acid sequestrant SFX
GI only because never enters systemic circulation
- -constipation, heartburn, nausea, belching, bloating, flatulence
- -decrease over time
bile acid sequestrant pregnancy category. why?
- relatively safe because never enters blood circulation, stays in GI tract
bile acid sequestrant that is used to tx pruritis r/t partial biliary obstruction
name the bile acid sequestrants
- cholesyramine [Questran]
- colestipol [Colestid]
- colesevelam [Welchol]
describe the esophageal risk of taking a bile acid sequestrant. how can this be prevented?
drug can expand in esophagus before getting to stomach/small intestine and cause esophageal blockage.
avoided by taking med with lots of water, other non-carb beverage, applesauce, or crushed pineapple
suffix used for all HMG-CoA reductase inhibitor drugs
antilipemic drug type that lowers LDL most effectively
(aka cholesterol synthesis inhibitors)
type of lipid most effected by statins
6 HMG-CoA reductase inhibitors
- lovastatin [ Mevacor]
- pravastatin [Pravachol]
- atorvastatin [Lipitor]
- fluvastatin [Lescol]
- rosuvastatin [Crestor]
- simvastatin [Zocor]
2 ways statins decrease LDL levels
- -decrease cholestrol synthesis
- -increase # of LDL receptors in liver, leading to more LDL being removed from blood
where cholesterol is made
- normally well-tolerated w/ few SFX
- -GI: mild and decrease over time
- -rhabdomyolosis, myopathy
- -elevations in liver enzymes (which may or may not be indicative of liver damage)
- -prolonged QT interval
breakdown of muscle fibers, usually d/t trauma or ischemia, but also as a potential SE of statins. contents of muscle cells spills into systemic circulation and can lead to acute renal failure
statin pregnacy category
X - teratogenic
how grapefruit juice interacts with statins
inhibits drug metabolism, leading to dangerously high serum drug levels
important labs to monitor for statins and why
- -liver enzymes: high levels could indicate liver failure
- -creatine kinase (not same as creatinine): enzyme released during muscle injury --> high levels could indicate rhabdomyolysis or myopathy
drugs that interact with statins
- erythromycin (antibiotic)
- gemfibrozil (antilipemic - fibric acid)
- niacin (antilipemic - nicotinic acid)
antihyperlipidemic with almost no effect on LDL (and no decrease in mortality r/t cardiovascular disease)? what is it used for?
fibric acid aka fibrate
used to tx hypertriglyceridemia, esp in combination with statins
2 fibric acid drugs and frequency of administration
- -gemfibrozil [Lopid] = 2x/day
- -fenofibrate [Antara, Tricor] = 1x/day
fibric acid SFX
- -GI: n/v/d
- -neuro: HA, peripheral neuropathy, decreased libido
- -allerigc rxns
- -gallstones (contraindicated in pts with gallbladder disease)
how fibrate works
(according to Saarman; book says mechanism unknown)
- -activates lipoprotein lipase, which breaks down cholesterol
- -suppresses release of FFA (free fatty acids) from adipose tissue
- -inhibits synthesis of triglycerides
- -increases secretion of cholesterol in bile
why wouldn't you give fibric acid to an immunocompromised pt?
causes decrease in WBC (and H&H)
fibric acid effect on liver enzymes
increases liver enzymes - b/c functions in the liver
vit B3 is the same thing as which antihyperlipidemic? how do doses compare?
b3 = niacin (aka nicotinic acid)
lipid-lowering doses are much higher than vitamin doses (~100x greater)
how does niacin work (according to Saarman; book says mechanism unknown)
- -increases activity of lipase, which breaks down lipids
- -reduces metabolism/catabolism of cholesterol and triglycerides
- -flushing, hot flashes in almost all pts, but can decrease this with ASA or other NSAID
- -GI distress
- -hyperglycemia (contraindicated in DM pts)
- -hyperuricemia (contraindicated in pts with hx of gout)
niacin interaction with statin or bile acid sequestrant
--> usually combined with one of these drugs and then used in lower doses to avoid adverse FX
Simcor is a combination of which two antihyperlipidemic classes
niacin + statin (simvastatin)