Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
29 Cards in this Set
- Front
- Back
- 3rd side (hint)
VLDL compose __ % of total blood cholesterol and most of the _______ measured
|
15-20; triglycerides
|
|
|
LDL contain __ % of total blood cholesterol, half of which are taken up by the _____ and ____ from circulation and the other half are taken up by _______
|
60-70; liver; removed; peripheral cells (including heart and vascular)
|
|
|
HDLs help in _____ of cholesterol from the ______ to the _______
|
transport; peripheral cells; liver
|
|
|
7 categories of anti-hyperlipidemics
|
Bile acid resins (BAR)
Niacin Fibric Acid Derivatives HMG-CoA reductase inhibitors Cholesterol absorption inhibitors Antioxidants Fish oils |
|
|
Bile acid resins (BAR) MoA
|
Binds bile acid, which are precursors to cholesterol (in the GI tract), preventing reabsorption
|
|
|
Clinical Ix for BARs?
|
Used for LDL reduction; no effect on triglycerides
|
|
|
BARs agts?
|
Cholestyramine & colestipol
|
|
|
BARs AEs?
|
Constipation, diarrhea, nausea, flatulence
|
|
|
Sig drug interactions of BARs?
|
Bind to many drugs in gut (admin 1 hr prior or 4 hrs after)
|
|
|
Nicotinic Acid (Niacin) MoA?
|
Inhibits release of free fatty acids from adipose -> decreased rate of lipoprotein synthesis
|
|
|
Nicotinic Acid (Niacin)clinical Ix?
|
Moderate reduction in LDL and moderate increase in HDL
|
|
|
Cx for Nicotinic Acid (Niacin)?
|
liver disease, peptic ulcers, & EtOH abuse
|
|
|
Fibric Acid Derivatives (Fibrates) MoA?
|
Elimination of triglyceride (TG) rich particles; helps w/ LDL & HDL moderately
|
|
|
Fibric Acid Derivatives (Fibrates) avail agts?
|
gemfibrozil & fenofibrate (both have "fibr" in their names)
|
|
|
Cx of Fibric Acid Derivatives (Fibrates)?
|
Severe hepatic or renal dysfunc
|
|
|
AEs of Fibric Acid Derivatives (Fibrates)?
|
N/V, abd pain, muscle weakness
|
|
|
D-D interactions of Fibric Acid Derivatives (Fibrates)?
|
W/ statins, increases risk of myopathy
|
|
|
All HMG CoA Reductase Inhibitors are:
|
statins
|
|
|
HMG CoA Reductase Inhibitors (statins) is most effective agent for:
|
LDL reduction; has moderate effect on HDL and TG
|
|
|
PKs & PDs of HMG CoA Reductase (statins) Inhibitors:
|
Dose dependent LDL reductions
Hepatically metabolized through 3A4 & 2C9 [1 exception] Highly protein bound Relatively short 1/2 lives w/ 2 exceptions |
|
|
1/2 life exceptions for HMG CoA Reductase Inhibitors (statins)?
|
ator- and rosu- (longer)
|
|
|
Metabolism exception for HMG CoA Reductase Inhibitors (statins)
|
prava- (renal elim)
|
Prague
|
|
Sig D-D interactions:
|
Cholestyramine (BAR) may decrease absorption
Inhibitors of 3A4 and 2C9 Displacement (resulting in more free [active] drug) |
|
|
Cholesterol Absorption Inhibitors MoA?
|
Inhibits chol. absorption by the small intestine
|
|
|
Cholesterol Absorption Inhibitors clinical Ix?
|
LDL reduction
|
|
|
Cholesterol Absorption Inhibitors agt?
|
Ezetimibe
|
|
|
Cholesterol Absorption Inhibitors Cx?
|
Active liver disease
Persistent elevation of liver enzymes |
|
|
Why aren't anti-oxidants used?
|
Insufficient evidence
|
|
|
Fish Oil use:
|
Secondary prevention in polytherapy in pts with increased non-HDL issues
SE is diarrhea |
|