What is an example of an HMG-CoA reductase inhibitor?
Atorvastatin ("statins")
What does atorvastatin do?
inhibits HMG-CoA reductase (enzyme) primarily responsible or hepatic synthesis of cholesterol
How would you describe atorvastatin?
It is the best class for lowering LDL cholesterol and TG while increasing HDL.
What is atorvastatin used for?
Used in patients that have hypercholesterolemia, and to reduce risk of CV events
When does atorvastatin peak after administration?
1-2 hours
What are adverse effects of atorvastatin?
* MYOPATHY*(muscle pain associated w statin use, if severe = RHABDOMYOLYSIS (life threatening bc muscle breakdown releases enzymes (creatinine kinase) that damage kidneys), watch out for dark coca colored urine), hepatic dysfunction, hyperglycemia
What is/are contraindications for statins?
pregnancy category X, take at night
What increases risks of statin side effects/toxicity?
- azole antifungals (fluconazole)
- macrolide abx (erythromycin)
- fibric acid derivatives (fenofibrate)
- grapefruit juice (CYP3A4 inhibitor)
What are examples of bile acid sequestrants?
cholesyramine
Where does cholesytamine work in the body?
in the intestines
What does cholestyramine do?
It binds to bile acids/salts, causing them to be excreted unchanged in the feces (= liver uses excess cholesterol to make new bile acids/salts instead of forming plaques in arteries)
How would you describe cholestyramine?
a bile acid/salt magnet
What is cholestyramine used for?
to decrease LDL (doesn't work too well for HDL/TG)
What are some adverse effects of cholestyramine?
it decreases efficacy of many orally taken drugs (esp statins), GI related (ex. N/V/D)
What would you do to allow absorption of orally taken drugs alongside cholestyramine?
give pt fat soluble vitamin supplements (A,D,E,K)
What is an example of a fibric acid derivative (fibrates)?
Fenofibrate
What does fenofibrate do?
decreases hepatic production of TG and VLDL cholesterol while increasing HDL.
How would you describe fenofibrate?
The best at lowering TG.
What kind of patients would use fenofibrate?
patients that have exceptionally high TG ( >500 md/dL) (they wld also have a very high risk of pancreatitis) associated with diabetes, gout, gastritis, or ulcer disease. Unnecessary otherwise (j use statins)
When does fenofibrate peak after administration?
at around 6-8 hours.
What are some adverse effects of fenofibrate?
increased risk of gallstones and bleeding from anticoagulants
What are some contraindications for fenofibrate?
patients with severe renal impairment or liver disease (fibrates can cause/worsen both)
Cholesterol Absorption Inhibitor
Ezetimibe (Zetia)
MOA: blocks biliary and dietary cholesterol absorption
Uses: dyslipidemia (monotherapy or in combo w statin)
NC: contraindicated in pregnant/lactating, not recommended in pts w severe hepatic impairment
PCSK9 Inhibitors
Alirocumab (Praluent)
MOA: increases activity of the receptors that clear cholesterol
Uses: Adults w ASCVD, family hc of hypercholesterolemia
NC: given subQ, well tolerated but VERY expensive
Niacin (Niacor, Niaspan)
U: no longer recommended
NC: only given to pts w high TG (>500). Data did not suggest pt outcomes improved.
AE: increases blood glucose and risk of hepatotoxicity.
BAD lab value for cholesterol?
>240
BAD lab value for LDL?
>160
BAD lab value for triglycerides?
>200
BAD lab value for HDL?
<40