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AU14 Pharmacology > Exam 3; Agents used to treat Hyperlipidemias > Flashcards

Exam 3; Agents used to treat Hyperlipidemias Flashcards

1
Q

What causes hyperlipidemia

A

a defect in the lipid transport system which provides cholesterol and triglycerides to the cell

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2
Q

There is an increased risk of these three things with an increase in blood lipids

A

coronary artery disease; due to increased plaque formation
pranceatitis
xanthoma; deposition of fat in the skin

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3
Q

This form on lipoprotein when in high levels, causes more potential problems

A

LDL; low density lipoproteins

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4
Q

What is the desirable level of LDL

A

< 100mg/DL

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5
Q

What converts chylomicrons ti free fatty acids

A

lipoprotein lipase

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6
Q

The chylomicron remnants (cholesterol) travel to which organ

A

the liver

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7
Q

These two things combine to form vLDL

A

apolipoprotein and cholesterol

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8
Q

What is the intermediate step in the formation of LDL from vLDL

A

vLDL → IDL → LDL

steps all catalyzed by lipoprotein lipase

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9
Q

If LDL becomes oxidized, what occurs

A

it is taken up by macrophage and deposited on arterial linings

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10
Q

What is a major carrier of cholesterol

A

LDL

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11
Q

LDL binds to what on the cell

A

LDL receptor

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12
Q

This enzyme in the cells can make cholesterol

A

HMG CoA reductase

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13
Q

Cholesterol can make these oh which can go into the gut

A

bile acids

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14
Q

What is considered the “good cholesterol”

A

HDL

high density lipoproteins

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15
Q

What four things cause secondary hyperlipoproteinemias

A

cirrhosis
alcoholism
nephrosis
diabetes

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16
Q

What are four things that cause primary hyperlipoproteinemias

A

decreased lipoprotein lipase
abnormal LDL receptors
over production of vLDL
decreased HDL synthesis

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17
Q

What are two non-pharmacologic treatments of hyperlipoproteinemias

A

diet/exercise

stop smoking

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18
Q

What are three mechanisms behind pharmacologic effects of drugs treating hyperlipoproteinemia

A

decrease production of lipoproteins
increase removal of lipoproteins/cholesterol
decrease absorption of lipoproteins

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19
Q

Can agents that treat hyperlipoproteinemias affect the fetus

A

Yes

20
Q

What will happen to the effects of hyperlipoproteinemia drugs upon stoppage of taking them

A

the effects will stop as well

21
Q

Which family of drugs are the HMG CoA reductase inhibitors

A

“-statin’s”

22
Q

True or False

the HMG CoA reductase inhibitors (-statins) are the most effective LDL lowering agents

A

True

23
Q

What is the mechanism of action behind the statin drugs

A

inhibits HMG CoA reductase; the rate limiting step in the cell synthesis of cholesterol

24
Q

When the cells cannot make their own cholesterol, how do they compensate

A

they increase the LDL receptors on the cell

25
Q

What is a major side effect of the statin drugs

A

myositis; muscle pain

especially true since many are metabolized by P450

26
Q

What are three side effects of statin drugs

A

liver toxicity
teratogenis; pregnancy category X
some memory loss

27
Q

What is the main difference between all the statin drugs

A

pharmacokinestics

28
Q

What is the mechanism of action behind niacin

A

it inhibits an enzyme essential for vLDL synthesis and may also bind to a receptor that decreases vLDL synthesis

29
Q

What is the result of using niacin

A

decrease in vLDL

increase in HDL; strongest increaser of HDL

30
Q

What are four side effects of Niacin

A

cutaneous flushing (red face)
itching
increased uric acid; gout
increase incidence of diabetes

31
Q

What are the three bile acid binding resins

A

cholestyramine
colestipol
coleselevam
“coles”

32
Q

What is the mechanism of action behind the “coles”

A

irreversibly bind to bile acids in the gut; are excreted along with their cholesterol

33
Q

What two things do the “cole” drugs cause

A

decrease in circulating cholesterol

increase in LDL receptors

34
Q

What are the side effects of the “cole” drugs

A

no side effects because they are not absorbed; but can cause nausea or GI irritants

35
Q

This family of drugs are the best triglyceride lowering agents

A

the fibrates

36
Q

What is the mechanism behind the fibrates

A

binds to PPAR; perixosome proliferator activating receptor

increasing the activity of LPL

37
Q

What are the fibrates

A

gemfibrozil
fenofibrate
(both have fibr)

38
Q

What are two side effects of gemfibrozil and fenofibrate

A

GI upset

can displace warfarin from plasma binding sites

39
Q

These two things decrease triglyceride synthesis via inhibition of an enzyme

A

omega 3 fatty acids

icosapent ethyl

40
Q

This essentially inhibits assembly of vLDL in the liver; both an enzyme and a transporter

A

imoitapide

41
Q

This is an anti-sense oligonucleotide

A

mipomersen

42
Q

What is the mechanism of mipomersen

A

binds to the mRNA for apoloprotein-B; preventing it from being synthesized

43
Q

This drug blocks cholesterol transport

A

ezetimibe

44
Q

This drug looks like cholesterol and blocks its uptake

A

sitostanl

45
Q

This inhibits GI and pancreatic lipase, decreasing fat absorption from the gut and causes loose stools

A

orlistat

46
Q

This is an non-absorbable oil used for frying/cooking but causes anal leakage → gross.

A

olestra

AU14 Pharmacology (29 decks)

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