Hyperlipidemia

1. What is our goal when treating someone with elevated lipids? Reducing these lipid levels (LDL)
& increase ↑ to reduce the risk of CHD. To decrease morbidity & mortality*.
2. Which cholesterol has been associated with poor patient outcome? LDL’s. When LDL receptors
decrease, LDL accumulates in blood and causes hypercholesteremia. LDL’s are mostly formed of
cholesterol.
3. Which Cholesterol is considered by many “good cholesterol?” High-density lipoprotein (HDL),
these have more protein content than lipid content.
4. What diseases are associated with the above and with elevated triglycerides?
o PANCREATITIS. Hypercholesterolemia, atherosclerotic plaque formation (which can lead
to CHF), cholesterol & coronary heart disease, hyperlipidemia, etc.
5. Which class or medications are considered the “drugs” of choice for treating elevated lipids
and why?
o HMG-CoA Reductase (Statins)- most effective/potent & ↓ MORBIDITY & MORTALITY
6. What is the mechanism by which the statins lower cholesterol levels? Statins aka HMG Co-
enzyme A Reductase Inhibitors. These lower blood cholesterol levels by decreasing the rate of
cholesterol production. The liver requires HMG-CoA to produce cholesterol since it is the rate
limiting enzyme in the rxns needed to make cholesterol. Statins INHIBIT this enzyme, thus ↓
cholesterol production, one of the last steps in cholesterol production.
7. After starting a statin when should cholesterol levels be rechecked? 6-8 weeks because that is
when max effects of statins are expected
8. Why is it important to know how a statin is metabolized? Most of the statins are drugs
metabolized by cytochrome P-450 enzyme (CYP3A4), HIV, & Hep C protease inhibitors,
grapefruit juice. These drugs have a lot of interactions. If any drug INHIBITS the action of enzyme
CYP, the levels of the statin will ↑. If other drug INDUCS the action of these p450 enzymes, then
Statins will be metabolized more and stain levels will ↓, cholesterol levels will ↑
9. AK is a 57 yo male taking Atorvastatin. He is to be started on erythromycin is that an issue?
Why or why not? If so, what will you do about it? Yes it is an issue because there is an
interaction between statins & erythromycin. This interaction will inhibit statin metabolism &
there will be a higher risk of pt experiencing myopathy.
10. NB is a 65 yo female started on Simvastatin after having an MI. She is being discharged from
the hospital. What should she be educated about? To immediately call provider if she
experiences any unexplained muscular pain or discomfort. Also, since she suffered an MI, if she
happens to be on an anticoagulant, drug interactions can occur & cause myopathy.
o Drug therapy knowledge, s/sx of adverse rxns, encourage lifestyle changes
o GI pain (due to possible liver damage)
o No grapefruit juice- interferes with P450
o Do not stop abruptly just because you are doing well
11. AS is a 72 yo to be started on Atorvastatin after having a cardiac cath. She asks what is the
best time of day to take it. What should she be told and why? It can be dosed at any time
 during the day, however, bedtime dosing provides peak drug levels in a time frame that
correlates better with the natural diurnal rhythm of cholesterol production in body
12. You are working in a medical office. OP is a 19 yo male with a family history of elevated lipids
and early MIs. His LDL is 250 mg/dl. He is started on atorvastatin. One week later he calls the
office and tells you he developed muscle aches and pains. What may be the cause of this?
What will you suggest to him? It could be myopathy OR rhabdo. Myopathy is an adverse rxn
that is associated with the use of statins. He most likely had a drug interaction if he happened to
take a drug that interacts with statins increasing the risk of myopathy. Pt would need to speak to
prescriber to see what other statin (risk vs benefit) he can take or get lower dose (if pain is
bearable). He may also be ordered to test CPK levels, depending on those levels then they can go
ahead and select another statin if convenient
13. In the hospital LT is being given Cholestryramine. What class does this belong to? What other
meds are in the class? How does it lower cholesterol levels? Cholestryramine is a bile acid
sequestrant. The other meds in this class are celestipol & colesevelam. These meds bind bile &
prevent the resorption of the bile acids form the small intestines. An insoluble bile acid & resin
(drug) complex is formed & excreted. Since bile acids are needed for cholesterol to be absorbed,
this is a natural way for the liver to excrete cholesterol. The more biles are excreted, the more
the liver converts cholesterol into bile acids ↓ cholesterol levels
14. The cholestyramine for LT comes from pharmacy in packets (powder). How should it be given?
This is a bile-acid sequestrant . The powder forms are inconvenient to use- taken in water. These
should not be taken with other drug due to reduced absorption. Also, other drugs should be
taken 1 hr before this drug or 4-6 hrs after taking this drug. Also, they should be taken with
meals to reduce adverse effects (constipation, nausea, belching, bloating) & w/ lots of fluid.
15. LT is also taking warfarin and digoxin. Any special concerns when also taking cholestyramine?
LT needs to make sure he takes these drugs an hr before taking cholestyramine or 4-6 hrs after-
it may reduce the absorption of these.
16. What side effects may be seen with cholestyramine and other bile acid sequestrants? Nasty
taste. Constipation. Nausea, belching, bloating, headaches, tinnitus, burnt odor of urine etc.
17. TG 45 yo hospitalized for pancreatitis from elevated triglycerides. A decision is made to start
the patient on fenobibrate. Why is this medication used vs a statin? Does it have any effect on
HDL? This med is a fibrate/fibric acid derivative. It primarily affects the TG levels but may also
lower total cholesterol & LDL’s & raises HDL’s. These activate lipoprotein lipase, an enzyme
responsible for cholesterol breakdown. Fibric acid derivatives also suppress free FA release from
adipose tissue, inhibit TG synthesis in liver, & increase the secretion of cholesterol onto bile.
18. TG who has also been taking warfarin has his INR done 2 weeks after starting fenofibrate.
Why may this lead to an elevated INR? Fibric acid derivative med enhance the action of oral
anticoagulants- decrease it clearance. (elevated INR= taking long to clot)
19. RW is a 64 yo taking 200 mg a day of niacin (100 mg BID). His practitioner dramatically
increased the dose. Why should have the dose been increased gradually over several weeks?
Niacin can cause adverse effects including, flushing (most commonly when you first start drug or
when you ↑ dosage) , pruritus, & GI distress. These can be minimized by starting pts on a low
 dosage & increasing it gradually & having pts take it with meals. Taking aspirin with it to prevent
a side effect.
20. What is the primary role for niacin with respect to treating lipid disease? Exact mechanism is
UK however it is believed to be related to its ability to inhibit lipolysis in adipose tissue, decrease
esterification of triglycerides in liver, & ↑ lipoprotein lipase (hydrolyzes lipoprotein) activity.
Decreases the VLDL production which leads to decrease in LDL
21. FL is supposed to start niacin, why should you tell him to take his daily dose of ASA 30 min
prior to the niacin? In order to minimize flushing (adverse effect) is is recommended to take
aspirin or an NSAID.
22. What side effects may be seen with niacin? Niacin can cause adverse effects including, flushing,
pruritus, & GI distress, ↑ glucose (DM), liver toxicity, muscle pain potentially, ↑ risk of GOUT
(just like thiazide diuretics)
23. You are perception a new nurse. She asks how does Ezetimbie lower cholesterol vs
Colesevelam. What should she be told? These are 2 different classes of drugs. Ezetimbie a
cholesterol absorption inhibiter; it selectively inhibits absorption of cholesterol & related sterols
in the small intestines. Colesevelam is a bile acid sequestrant & these meds bind bile & prevent
the resorption of the bile acids form the small intestines. An insoluble bile acid & resin (drug)
complex is formed & excreted. Since bile acids are needed for cholesterol to be absorbed, this is
a natural way for the liver to excrete cholesterol. The more biles are excreted, the more he liver
converts cholesterol into bile acids ↓ cholesterol levels. They both lower cholesterol levels
but in different ways.
24. KY is a 44 yo female with elevated cholesterol levels. He has been taking drug therapy for 2
years and his cholesterol finally hit the desired level so he has stopped the medication. Is that
a good or bad idea and why? Bad idea. He should continue it because if not it will go back to the
same levels as before.
25. What fish oil supplements are approved to treat lipid disorders? Omega-3-FA (an essential
fatty acid). Lovaza reduces cholesterol.
26. What lipid disorder are they approved for? Triglycerides.