Flashcards in L24 Deck (32):
Receptor for HDL on liver for steroidogenic tissues
What drug class is the most effective at reducing LDL
Statin mechanism of lowering cholesterol
X HMG co-reductase
- No cholesterol synthesis
More LDL-R expression b/c less LDL in circulation - sensitizes the system
Statin mechanism for CV benefits
How are most statins metabolized? Exceptions?
First pass extraction in liver via CYP enzymes
- Rosuva only slightly metab by liver
Statin adverse SEs
1. Hepatitis that presents as flu-like sickness
2. Rhabdomyolysis - can progress to kidney failure
3. New onset diabetes
4. Teratogenic - don't give to pregnant women
5. Peripheral neuropathy
6. cP450 drug ints
What 2 enzyme levels are you going to monitor for pts on statins
Serum liver transaminases
Should you give statins to diabetic pts?
Higher risk of experiencing a cardiac event or death if diabetic
But benefits >> risk
When should pts take their statins?
Cholesterol levels highest at night
What are the 3 1st gen statins?
What are the 2, 2nd gen statins?
More potent forms
What is the mechanism of bile acid binding resins?
Bile acids contain cholesterol
- Usually recycled to preserve cholesterol stores
Instead, bind them and excrete them
Force the liver to use cholesterol to make more
Less cholesterol in circulation, reflex increase LDL-R expression
Which pts should you NOT give bile acid binders to?
Bide acid binders also increase VLDL for unknown reasons --> increases TGs
Bind acid binder SEs
Name the 2 bile acid binding resins
Which cholesterol absorption inhibitor do you need to know
Blocks cholesterol and plant sterol GI absorption via X NPC1L1
Acts on dietary AND biliary cholesterol
No change to TGs
How is ezetimibe excreted
Feces - with whatever it bound!
Evidence shows ezetimibe acts best when added to which statin specifically
3 PCSK9 inhibitors you need to know
PCSK9 inhibitor mechanism
PCSK9 = internalization of LDL-R
Give w/ statins b/c when you ↑LDL-R, you also ↑PCSK9 levels
What is a gain of function PCSK9 mutation associated with?
What disease is secondarily benefited by ↓LDL
Ligand for peroxisome proliferator-activated receptor (PPAR)
= nuclear receptors
↓TG + ↑HDL
2 fibrates you need to know
Use of fibrates
BEST method to ↓TGs
Which drug interaction should you keep in mind with fibrates?
Adjust dosing since fibrates bind plasma proteins warfarin would otherwise bind
↑risk gallstones b/c ↑biliary cholesterol
Which drug will give the largest ↑HDL
Nicotinic acid (this is the active form)
Also some ↓LDL & TGs
Nicotinic acid mechansim
Activates Niacr1 on adipose tissue
X lipolysis --> no FFAs toliver for TG or VLDL synthesis
Is there a benefit to combining niacin w/ statins?
No - niacin goal is not for LDL reduction
Use alone to ↓TGs