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Flashcards in Lipids Deck (23)
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1

total cholesterol

<200mg/dL

2

LDL

<130mg/dL

3

HDL

>60mg/dL

4

VLDL

not measured

5

LDL:HDL RATIO

3.0-3.5:1

6

LP(a)

-

7

triglycerides

<165mg/dL

8

bile acid sequestering agents

cholestyramine, cholestipol

9

nicotinic acid

niacin

10

HMG co-A reductase inhibitors

lovastatin, simvistatin, pravastatin, fluvastatin, atorvastatin, cerivastatin

11

fibric acid derivatives

gemfibrozil, clofibrate, fenofibrate

12

bile seq agents MOA

1. binds to bile acids in sm intestine (poop out)
2. liver must use intracellular chol stores to make more bile acids
3. to replenish intracellular chol, liver takes in more plasma chol=lower plasma cholesterol (LDL)

13

niacin MOA

1. inhibits lipolysis in adipocytes
2. so decreased hepatic VLDL synthesis
3. so decreased VLDL==decreased LDL

14

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

15

Fibrates MOA

increase lipoprotein lipase=decrease plasma cholesterol
decrease apo C2=decrease plasma cholesterol
increased expression of apo A1 & 2=increase in plasma HDL

16

Omega-3-Acid Ethyl Esters MOA

reduce synthesis of triglycerides in liver by limiting enzymes

17

bile seq agents effects

-significant LDL lowering effects (less than statins)
-small increase in HDL
-little to no effect TG

18

HMG CoA reductase inhibitors (statins) effects

-significant (BEST) LDL lowering effects
-modest increase in HDL
-modest decrease TG

19

Fibrates effects

-small LDL lowering effect
-significant HDL increase
-significant TG decrease

20

Niacin effects

-modest decrease LDL
-significant HDL increase
-significant TG decrease

21

metabolic syndrome

at least 3 of the following:
1. increased abdominal circumference
2. elevated BP
3. elevated TG
4. elevated sugar
5. decreased HDL

22

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

23

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