agents used to treat hyperlipidemias Flashcards

1
Q

hyperlipidemia

A

defect in lipid transport system that provides cholesterol and triglycerides to the cell.

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2
Q

hyperlipidemia leads to what

A

increase risk for coronary artery disease
increase risk of plaque formation in vascular
increase risk of pancreatits
increase risk of xanthoma

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3
Q

LDL stands for what

A

low density lipoprotein

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4
Q

how much LDL should you have

A

<100 mg/DL

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5
Q

secondary hyperlipoproteinemias

A

environmental causes
alcholoism- cirrhosis
diabetes- nephrosis

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6
Q

primary hyperlipoproteinemias.

A
genetic abnormalities 
decrease in lipoprotein lipase
abnormal LDL receptors
overproduction of VLDL 
decrease in HDL synthesis
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7
Q

treatment of hyperlipidemias

A

non-pharmacologic- diet, weight loss, aerobic exercise, stop smoking
also pharmacologic

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8
Q

decreasing fats in diet = decrease in what

A

cholesterol

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9
Q

pharmacologic treatment of hyperlipidemias

A

decrease production of lipoproteins
decrease absorption
increase removal of lipoproteins
(all effective with oral admin)

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10
Q

what is the most effective LDL lowering agent?

A

HMG CoA reductase inhibitors- lovastatin, “statin”s

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11
Q

lovastatin mech of action

A

prodrug

HMG CoA reductase- rate limiting step in cell synthesis of cholesterol

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12
Q

if cells can’t make any of their own cholesterol what happens?

A

find another way to get more LDL- increase LDL receptors of the cell = increase in LDL uptake (25%- 60%).

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13
Q

SE of lovastatin

A
  • myositis (muscle pain) -> rhabdomyolysis (total breakdown of muscle)
  • liver toxicity
  • teratogenic pregnancy category X
  • some memory loss
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14
Q

fats go into the gut and come out as _____ containing _____ and _____

A

chylomicrons, triglycerides, cholesterol

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15
Q

fate of chylomicrons

A
  • lipoprotein lipase convert to free fatty acids that go to the cell
  • remnants go to liver
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16
Q

chylomicrons remnants in the liver and do 2 things

A
  1. bind with apolipoprotein B and make VLDL

2. relased from liver as bile acids into the gut

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17
Q

liver also produces _____ that is ultimately reabsorbed by it

A

HDL

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18
Q

fate of VLDL

A

lipoprotein lipase takes of triglycerides = IDL,

Lplipase takes off more stuff = LDL

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19
Q

LDL is major carrier of what

A

cholesterol

20
Q

fate of LDL

A
  1. oxidized and taken up by macrophages and deposited on arterial lining
  2. bind to LDL receptors on cell membrane where its converted to cholesterol
21
Q

another way to make cholesterol in the cell

A

HMG CoA reductase

22
Q

what is niacin?

A

vitamin B3

23
Q

mechanism of action of niacin

A
  1. inhibits an enzyme essential for VLDL synthesis

2. bind to receptor that decreases VLDL synthesis

24
Q

T/F niacin is best increaser of HDL

A

True

25
Q

ultimately niacin increases what and decreases what

A

increases HDL, decrease VLDL

26
Q

SE of niacin

A

cutaneous flushing “red face”
itching
increase uric acid-gout
increase incidence of diabetes

27
Q

drugs that bing to bile acid

A

cholestyramine
colestipol
coleselevam

28
Q

mech of action of bile acid binding resins

A

irreversibly bind to bile acids in gut causing them to be excreted with their cholesterol

29
Q

outcome of taking bile acid binding agents

A

decreases circulating cholesterol

increases LDL receptors

30
Q

do you have to take a lot of this drug to be effective?

A

yes 5-30g a day

31
Q

SE of bile acid binding resins

A

no systemic cuz too big to be absorbed
can bind to acidic drugs like oral anticoagulants and digoxin
decrease absorption of fat soluble vitamins
nausea

32
Q

agents that decrease cholesterol absorption by the intestines

A
SOOE
Sitostanol
orlistat
olestra
ezetimibe
33
Q

ezetimibe

A

blocks cholesterol transporter

34
Q

sitostanol

A

looks like cholesterol, blocks uptake

35
Q

orlistat

A

inhibits GI, pancreatic lipase, decreases fat absorption in gut, major problem is loose stools

36
Q

fibrates

A

best triglyceride lowering agents, bind to PPAR

37
Q

fibrate drugs

A

gemfibrozil, fenofibrate

38
Q

mech. of action of fibrates

A

increase transcription of lipoprotein lipase- decrease in triglycerides and VLDL

39
Q

what can you not take with fibrates

A

warfarin- displaces it.

40
Q

omega 3 fatty acids

A

decrease triglyercide synthesis, by inhibiting enzymes

41
Q

omega 3 FA drug

A

icosapent

42
Q

lomitapide

A

inhibits assembly of VLDL in liver

both enzyme and a transporter

43
Q

SE of lomitapride

A

hepatoxicity

44
Q

other hyperlipidemias

A

lomitapide

mipomersen

45
Q

mipomersen

A

amhistase oligonucleotide

binds to RNA for APOb and prevents synthesis of APO