lipid management Flashcards
(38 cards)
Macromolecular complexes in the blood that transport lipids
lipoproteins
Proteins on the surface of lipoproteins; they play critical roles in
the regulation of lipoprotein metabolism and uptake into cells
apolipoproteins
Cholesterol-rich lipoprotein whose regulated
uptake by hepatocytes and other cells requires functional LDL receptors; an
elevated LDL concentration is associated with atherosclerosis
Low-density lipoprotein (LDL):
Cholesterol-rich lipoprotein that transports
cholesterol from the tissues to the liver; a low concentration is associated with
atherosclerosis
High-density lipoprotein (HDL)
essential to normal body functions and involved in synthesis of bile
salts, cell membranes, hormones, vitamin D
Cholesterol
Triglyceride and Cholesterol-rich lipoprotein
secreted by the liver that transports triglycerides to the periphery; precursor of
LDL
Very-low density lipoprotein (VLDL)
3-Hydroxy-3-methylglutaryl-coenzyme A reductase; the
enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis
HMG-CoA reductase
An enzyme found primarily on the surface of endothelial
cells that releases free fatty acids from triglycerides in lipoproteins; the free fatty
acids are taken up into cells
Lipoprotein lipase (LPL)
Member of a family of nuclear
transcription regulators that participate in the regulation of metabolic processes;
target of the fibrate drugs and omega-3 fatty acids
Proliferator-activated receptor-alpha (PPARα)
transport cholesterol and triglycerides from GI
tract to body
Chylomicrons
TG-rich lipoproteins, precursor to LDL
VLDL
major source of atherosclerosis, very rich in cholesterol
LDL
high levels may reduce atherosclerosis, removes
cholesterol from the periphery and brings it to the liver for
breakdown
HDL
- Injury to vessel lining:
o High BP
o Smoking
o High LDL and triglycerides - After initial damage: fat, cholesterol, platelets, etc. begin a cycle
o Leads to accumulation around the lining of arteries
Leads to cardiovascular disease
atherosclerosis
testing lipids
FLP = fasting lipid profile
o Total cholesterol
o LDL
o HDL
o Triglycerides
o Age 20+ every 4-6 years, annually for higher risk patients
o Frequency also affected by FH (diabetes, stroke, etc.
Calculating LDL
o Friedwald equation: LDL = TC - (HDL + (trigs/5))
o Not accurate when trigs > 400
Primary Treatment Goal:
Lower the risk of cardiovascular events (CVD), including heart attacks and
strokes
Target Lipid Levels
o LDL cholesterol goal: <100 mg/dL (lower for high-risk patients)
o HDL cholesterol: Higher is better (>60 mg/dL), exercise and weight loss
raises
o Triglycerides: <150 mg/dL
Non-Pharmacologic Approaches:
o Diet: Reduce saturated fats, increase omega-3s
o Exercise: At least 150 minutes per week of moderate-intensity aerobic activity
o Weight loss
mainstay in atherosclerotic CVD
prevention
Lifestyle modification
Most common and effective drug class to lower LDL
Statins (HMG-CoA Reductase Inhibitors): “statins”
* Benefits: Decrease LDL, reduce inflammation, stabilize plaques
Examples:
o Atorvastatin (Lipitor)
o Rosuvastatin (Crestor)
- MOA
o Structural analogs of HMG-CoA with a strong affinity for HMG-CoA
reductase
Rate limiting step in de novo cholesterol synthesis
o ᾆInhibit cholesterol synthesis
Deplete intracellular cholesterol reducing circulating LDL
o ᾆIncrease cell-surface LDL receptors that bind and internalize
circulating LDL
Further decreases cholesterol
o Also stabilize plaques, inhibit platelet thrombus formation, and have
anti-inflammatory effects
statins
Statins ADR
myalgia
hepatotoxicity
Ask patient to report muscle symptoms, brown urine (Coca Cola
colored)
Usually in patients with renal insufficiency or those taking certain
drugs: Gemfibrozil, Niacin
Statins
DDIs
- Grapefruit interacts with Atorvastatin, Simvastatin, Lovastatin
o These are CYP3A4 substrates - Rosuvastatin is CYP2C9 substrate
- Pravastatin is not metabolized by CYP450
