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IC > Treatment of Hyperlipidemias > Flashcards

Treatment of Hyperlipidemias Flashcards

1
Q

Lipoproteins

A

high mw complexes of specific proteins and lipids; transport triglycerides and cholesterol in the blood

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2
Q

lipids used for

A

energy production (triglycerides) and membrane synthesis (cholesterol)

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3
Q

larger, less dense lipoproteins contain

A

more triglycerides

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4
Q

chylomicrons

A

only lipoproteins that have apolipoprotein b48

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5
Q

Exogenous pathway

A

chylomicrons synthesized in enterocytes transport dietary lipids from circulation
20% of body’s cholesterol from food

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6
Q

Endogenous pw

A

VLDL synthesized in hepatocytes transports FA and cholesterol to peripheral tissues
80% of body’s choletserol
Affected by dietary fat intake

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7
Q

LDL

A

longest half life
70% of total plasma cholesterol
elevated is a major RF for atherosclerosis
migrates into vascular intima and can form plaques

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8
Q

HDL

A

draws free cholesterol from cholesterol rich cells and takes it back to liver “reverse cholesterol transport” and transformed into bile or vldl
-synthesized by liver
-

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9
Q

Lp(a) lipoprotein

A

Formed from LDL and apo(a)

can be found in plaques

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10
Q

Primary hypertriglyceridemia

A

High triglycerides (200-500 mg/dL)

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11
Q

Familial hypertriglyceridemia

A

develops with age, weight gain, diabetes

Tx dietary, weight reduction, exercise

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12
Q

Rare primary hypertriglyceridemia

A

Familial lipoprotein lipase def

ApoCII def

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13
Q

Primary hypercholesterolemia

A

High cholestserol (250-500 mg/dl) w. normal triglycerides (150 mg/dL)

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14
Q

Familial hypercholesterolemia

A

defects in LDL receptor
elevated cholesterol levels from birth- requires treatment
Responds well to statins and lipid lowering drugs

-homozygous is rare- levels of 1000 mg/dl possible- cardiovascular disease in childhood

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15
Q

Familial defective apoB100

A

mutation leads to dec affinity to LDL receptor

responds well to statins and niacin

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16
Q

Mixed hyperlipidemia

A

elevated total cholestero, ldl, triglycerides

hdl reduced

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17
Q

familial combined hyperlipidemia

A

common
w/ obesity, hyperinsulinemia, glucose intolerance
statins, combined maybe with fibrates and niacin

18
Q

Dysbetalipoproteinemia

A

defects in apoE

inc cholymicrons and IDL-like particles; tx- decrease fat and cholesterol intake; niacin and fibrates

19
Q

LDL, cholesterol, hdl levels

A

LDL <100 optimal
Total <200 desirable
HDL >60 good

20
Q

4 groups of ppl that should be treated with statin

A

individuals with:

1) clinical atherosclerotic cardiovascular events
2) LDL-c >190 mg/dl
3) 40-74 years of age with diabetes with LDL-c 70-189 mg/dl
4) 40-75 years w/o atherosclerosis with LDL 70-189 and estimated ASCVD risk of 7.5% or higher

21
Q

HDL apolipoprotein

A

A, C, E

22
Q

HMG-CoA reductase inhibitors

A
  • statins
  • atorvastatin, fluvastatin, rosuvastatin, pravastatin (active drugs)
  • lovastatin, simvastatin (prodrugs)
  • inhibit HMG-CoA reductase to reduce hepatic formation of cholesterol and increase LDL receptors in hepatocytes to lower plasma LDL
  • decrease plasma triglycerides and increase HDL
  • all have high first pass hepatic extraction and most excreted in bile
23
Q

Niacin

A

nicotinic acid, vit b3

24
Q

fibric acid derivatives

A

gemfibrozil and fenofibrate

25
Q

bile acid binding resins

A

colestipol, cholestyramine, colesevelam

26
Q

intestinal sterol absorption inhibitor

A

ezetimibe

27
Q

pleiotropic statin effects

A

-reversal of endothelial dysfunction- improved response to NO
-dec inflammation
dec coagulation
improved plaque stability

28
Q

therapeutic uses for statins

A

elevated LDL levels
reduce mortality from MI and CVD pts at high risk
best given at night when most cholesterol synthesis occurs
contra in pregnancy

29
Q

statin toxicity

A

hepatic toxicity

-indicated by elevations in serum aminotransaminase

30
Q

statin metabolized by CYP3A4

A

atorvastatin, lovastatin, simvastatin

31
Q

statin metabolized by CYP2c9

A

fluvastatin and rosuvastatin

32
Q

what statin is not metabolized by p450

A

pravastatin

33
Q

statin toxicity other

A

skeletal muscle- increased creatinine kinase activity
-low dose, lower AE

  • when combining with fibrates (gemfibrozil) will increase rhabdomyolysis
  • measure serum aminotransferase and creatinine kinase
  • no simvastatin and amiodarone together because of rhabdomyolysis
34
Q

Niacin

A

water soluble B3 vitamin converted to the amide
-large doses improve every lipid parameter
-reduce ffa flux to liver
-dec hepatic synthesis of trglycerides and vldl
-lower plasma ldl
-most effective for elevating hdl
will cause some cutaneous flushing (inc prostaglandins)

35
Q

Fibric acid derivatives

A

Gemfibrozil and fenofibrate
ligands for PPAR-alpha in hepatocytes (peroxisome proliferator activated receptor alpha)
-activation decreases plasma triglycerides, VLDL and LDL and increases plasma HDL
-used for hypertriglyceridemia and dysbetalipoproteinemia

36
Q

Fibric acid derivatives toxicities

A 
skin rashes
gi symptoms
dec in wbc or hematocrit
rarely rhabdomyolysis 
avoid in pts with hepatic or renal dysfunction
modest risk of cholesterol gallstones 
myopathy inc in combo with statins
37
Q

omega 3

A

activate pparalpha

reduce triglycerides

38
Q

bile acid binding resins

A

colestipol, cholestyramine, colesevelam

  • bind bile acids and increase excretion
  • used in primary hypercholesterolemia, might result in inc of vldl, may be used for treating digoxin toxicity

no systemic effects- no side effects
may decrease absorption of vitamins adek
impair absorption of certain drugs like digoxin, thiazides, tetracyclin, fluvastatin, thyroxne, aspirin

39
Q

ezetimibe

A

inhibits intestinal absorption of cholesterol and phytosterols
-reduces ldl and minimal inc in hdl
-tx of primary hypercholesterolemia
low incidence of reversible hepatic impairment

40
Q

simcor

A

extended release niacin plus simvastatin

41
Q

vytorin

A

ezetimibe plus simvastatin

IC (31 decks)

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