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Nurs 5229 Clinical Pharmacotherapeutics > Lipid Lowering Agents > Flashcards

Lipid Lowering Agents Flashcards

1
Q

Most effective drugs for lowering LDL

A

HMG-CoA Reductase

Inhibitors (Statins)

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2
Q

• Nonlipid beneficial cardiovascular actions of statins

A

– Promote plaque stability
– Reduce the risk for cardiovascular (CV)
events

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3
Q

Statins can show

A
  • Reduction of LDL cholesterol
  • Elevation of HDL cholesterol
  • Reduction of triglyceride levels
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4
Q

Statin MOA

A 
Mechanism of
action:
-Competitive
inhibitors of
hydroxymethylgluta
ryl (HMG) CoA
reductase, the ratelimiting step in
cholesterol
biosynthesis.

***Increase the # of
LDL receptors on
hepatocytes.

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5
Q

Statins should be adminstered in the

A

evening – cholesterol synthesis

normally increases during the night

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6
Q

Statins have a significant

A

first pass effect

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7
Q

Lovastatin absorption is increased

A

food

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8
Q

statin ADR

A

Common – headache, rash,
GI disturbances
• Rare AE: myopathy/rhabdomyolysis,
hepatotoxicity.

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9
Q

Stain interactions

A

Drug interactions

– With other lipid-lower drugs, drugs that inhibit CYP3A4.

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10
Q

Statin routine monitoring of

A

f serum creatine

kinase (CK) levels is not recommended.

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11
Q

Check baseline aminotransferase levels

prior to initiating

A

statin therapy; do not

routinely monitor when on statins

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12
Q

Recheck lipid panel

A

6 to 8 weeks after

initiation or change of treatment

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13
Q

Hepatic Dysfunction

in statin therapy - Clinical studies -

A

0.5 to 3.0 percent occurrence of
persistent elevations in aminotransferases,
primary in the first 3 months, dose dependent.
• Rare – severe liver injury (typically 3 to 4 months
after initiation).

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14
Q

statin previous ____

A

LFT prior to initiation (routine monitoring

of LFT now not necessary).

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15
Q

ALT level more than 3x the upper level of
normal, confirmed on two occasions.
– Use different

A

statin, dose reduction, alternative day

therapy

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16
Q

Statin can cause

A

muscle adverse events

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17
Q

mild muscle injury

A

muscle aches, tenderness, or
weakness can localize to certain muscle
groups or be diffuse.

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18
Q

myositis

A

– muscle inflammation, moderate

elevation of CK

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19
Q

rhabdomyoloysis

A

– muscle disintegration

or dissolution.

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20
Q

• If patient reports muscle symptoms,

A

btain

a CK blood level

21
Q

• CK value is > 10x increase

A

ULN: stop

therapy

22
Q

CK value is < 10x increase ULN

A

can
continue, follow symptoms and CK level
weekly, OR stop and re-evaluate

23
Q

• Routine monitoring of CK in asymptomatic

patients is

A

not necessary.

24
Q

Niacin uncommonly

A

Uncommonly used – lower LDL

25
Q

Niacin increases

A

• Increases HDL levels
– Does little to improve outcomes – AIM-HIGH trial
2011

26
Q

Niacin combo with __ no longer used

A

Combo of niacin with statin – no longer used

27
Q

Niacin concerns about

A

Concerns about niacin monotherapy (AIMHigh trial)

28
Q

Niacin can rais

A

Can raise HDL – but generally no recommendation to use for this

29
Q

Niacin use is alos

A

limited as it is not well-tolerated

30
Q

niacin ADR

A

– Skin (flushing, itching)
• Intense flushing initially; can pretreat with aspirin
325mg 30 minutes before each dose.
***Decreased with sustained-release (SR) version of
niacin

– Gastrointestinal (gastric upset, n/v, diarrhea)
– Hepatotoxicity (severe liver damage has
occurred) – baseline LFTs, and monitor
– Hyperglycemia
– Gouty arthritis

31
Q

Niacin baseline ___ should be obtained and monitored

A

LFT

32
Q

Bile Acid Sequestrants MOA

A

MOA: bind bile acids in the intestine, resulting in

interruption of the reabsorption of bile acids

33
Q

Bile Acid Sequestrants reduction in

A

Reduction in cholesterol pool lowers intrahepatic
cholesterol, promotes synthesis of LDL receptors.
Receptors bind LDL from the plasma, causing
further reduction in blood cholesterol.

34
Q

Bile Acid Sequestrants reduce

A

Reduce LDL cholesterol levels

35
Q

Bile Acid Sequestrants used primarliy as adjucts to

A

Used primarily as adjuncts to statins.

36
Q

Bile Acid Sequestrants use often limited as

A

side effects – GI (nausea,

bloating, cramping, increase in liver enzymes)

37
Q

Cholesterol Absorption Inhibitor - Ezetimibe

A

– Impairs dietary and biliary cholesterol
absorption at he brush border of the intestines
– Most commonly prescribed to lower LDL-C after statins

38
Q

Cholesterol Absorption Inhibitor theraputic use

A

– Reduces total cholesterol, LDL cholesterol,
and apolipoprotein B
– Approved for monotherapy and combined use
with statins

39
Q

Fibric Acid Derivates (Fibrates) most effective

A

• Most effective drugs available for lowering TG levels (as

much as 50%

40
Q

Fibric Acid Derivates (Fibrates) can raise

A

Can raise HDL cholesterol

41
Q

Fibric Acid Derivates (Fibrates) little or no effect

A

• Little or no effect on LDL cholesterol

42
Q

Fibric Acid Derivates (Fibrates) can increase the risk for

A

Can increase the risk for bleeding in patients taking

warfarin

43
Q

Fibric Acid Derivates (Fibrates) can increase the risk for

A

• Can increase the risk for rhabdomyolysis in patients

taking statins

44
Q

Fibric Acid Derivates (Fibrates) three durgs in US

A

– Gemfibrozil [Lopid]
– Fenofibrate [Tricor, others]
– Fenofibric acid [TriLipix

45
Q

Fibric Acid Derivates ADR

A

Adverse effects: have been associated
with muscle toxicity and is more profound
with those patients also treated with a
statin.

46
Q

Fibric Acid Derivates ADR effect can be medicated by

A

Effect can be mediated by a competitive

inhibition of CYP3A4.

47
Q

Fibric Acid Derivates safer options

A

Pravastatin and Fluvastatin are NOT
extensively metabolized by the CYP3A4
• Maybe safer when combination therapy is required
with a fibrate, but this is not certain

48
Q

Fibric Acid Derivates interactions

A

Interactions – interfere with the
metabolism of warfarin (warfarin should be
reduced by 30% in these patients).

Nurs 5229 Clinical Pharmacotherapeutics (78 decks)

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