Lipids Flashcards
total cholesterol
<200mg/dL
LDL
<130mg/dL
HDL
> 60mg/dL
VLDL
not measured
LDL:HDL RATIO
3.0-3.5:1
LP(a)
-
triglycerides
<165mg/dL
bile acid sequestering agents
cholestyramine, cholestipol
nicotinic acid
niacin
HMG co-A reductase inhibitors
lovastatin, simvistatin, pravastatin, fluvastatin, atorvastatin, cerivastatin
fibric acid derivatives
gemfibrozil, clofibrate, fenofibrate
bile seq agents MOA
- binds to bile acids in sm intestine (poop out)
- liver must use intracellular chol stores to make more bile acids
- to replenish intracellular chol, liver takes in more plasma chol=lower plasma cholesterol (LDL)
niacin MOA
- inhibits lipolysis in adipocytes
- so decreased hepatic VLDL synthesis
- so decreased VLDL==decreased LDL
HMG CoA reductase inhibitor MOA
in liver, HMG CoA reductase is required to make cholesterol de novo–statins inhibit this, lowering intracellular cholesterol, increasing LDL receptors and uptake of LDL out of the blood; also lowers secretion of VLDL into blood
Fibrates MOA
increase lipoprotein lipase=decrease plasma cholesterol
decrease apo C2=decrease plasma cholesterol
increased expression of apo A1 & 2=increase in plasma HDL
Omega-3-Acid Ethyl Esters MOA
reduce synthesis of triglycerides in liver by limiting enzymes
bile seq agents effects
- significant LDL lowering effects (less than statins)
- small increase in HDL
- little to no effect TG
HMG CoA reductase inhibitors (statins) effects
- significant (BEST) LDL lowering effects
- modest increase in HDL
- modest decrease TG
Fibrates effects
- small LDL lowering effect
- significant HDL increase
- significant TG decrease
Niacin effects
- modest decrease LDL
- significant HDL increase
- significant TG decrease
metabolic syndrome
at least 3 of the following:
- increased abdominal circumference
- elevated BP
- elevated TG
- elevated sugar
- decreased HDL
Familial hypercholesterolemia
cell surface receptors for LDL molecule absent/defective=unregulated synth of LDL
homozygotes: ~8x normal level of LDL (atherosclerotic disease in childhood)
heterozygotes: ~2x normal LDL, develop CHD in 30’s or 40’s
familial hyperchylomicronemia
abnormality of lipoprotein lipase (enzyme that enables peripheral tissues to take up TG from chylomicrons and VLDL particles)
-these patients have marked hyperTGemia with recurrent pancreatitis and hepatosplenomegaly in childhood