Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Fall 2014 - Pharm Cardio > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What is the non-pharmacologic therapy for dyslipidemia?

A

lifestyle modifications: healthy diet, weight loss, exercise, stop smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the pharmacologic options for dyslipidemia?

A
  • statins
  • fibric acids
  • bile acid resins
  • nicotinic acid
  • 2-azetidione
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is another name for the statin drug class?

A

-HMG CoA Reductase Inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What it the statin MOA?

A
  • inhibit HMG CoA reductase, which is an enzyme in cholesterol production
  • statins reduce, but don’t completely block, cholesterol synthesis
  • increase LDL catabolism
  • also have anti-inflammatory activity (decrease CRP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Adverse Effects of Statins

A
  • hepatic toxicity
  • myopathy (myalgia, myositis, rhabdomyolysis)
  • neuropathy
  • small increased risk of DM at high doses
  • non-serious and reversible cognitive side effects (memory loss, confusion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Statin CI

A
  • pregnancy (cat X) and lactation
  • active or chronic liver dz
  • concomitant use of CSA (cyclosporin A), gemfibrozil, niacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Drug Interactions of Statins

A
  • reports of myopathy when administered with CSA, gemfibrozil, clofibrate, niacin, azole antifungals, erythromycin, nefazodone, protease inhibitors
  • may potentiate oral anticoagulants
  • increased effect/toxicity of levothyroxine (thyroid med)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What kind of dose-response relationship do statins have?

A

-non-linear: substantial reduction in LDL at starting doses; each doubling of dose reduces LDL 6% more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When is dosing of statins most effective?

A

evening dosing usually yields greater effects on LDLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which statins have the most drug interactions?

A

lovastatin and simvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MOA of Bile Acid Resins

A
  • increase LDL catabolism

- decrease cholesterol absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

AEs of Bile Acid Resins

A

-GI SXS MOST COMMON

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bile Acid Resins CI

A
  • monotherapy for TGs > 500 MG/DL
  • familial dysbetalipoproteinemia
  • hx of severe constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Bile Acid Resins Drug Interactions

A
  • binds with many coadministered acidic drugs (eg warfarin, NSAIDs, beta blockers)
  • take 1 hour before or 4 hours after
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Fibric Acid MOA

A
  • increase VLDL clearance

- decreased VLDL synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Fibric Acid AE

A
  • GI complaints most common

- can increase bile lithogenicity

17
Q

Fibric Acid CI

A
  • hepatic or severe renal dysfunction

- pre-existing gallbladder dz

18
Q

Nicotinic Acid/Niacin MOA

A

-decrease LDL and VLDL synthesis

19
Q

Nicotinic Acid/Niacin AE

A
  • flushing most common
  • may cause glucose intolerance and increase uric acid levels
  • hepatotoxicity
20
Q

Nicotinic Acid/Niacin CI

A
  • liver disease
  • type 2 DM
  • hout
  • hyperuricemia
21
Q

Ezetimibe MOA

A

blocks cholesterol absorption

22
Q

Ezetimibe AE

A

-may cause fatigue, abd pain, diarrhea, arthralgia, back pain

23
Q

Ezetimibe CI

A

-combination with statins in active liver dz or pts with persistent LFT elevations

24
Q

Which dyslipidemia class is best at reducing LDL?

A

statins

25
Q

Which dyslipidemia class is best at reducing TG?

A

fibric acids and nicotinic acid/niacin

26
Q

Which dyslipidemia class is best at increasing HDL?

A

niacin/nicotinic acid

27
Q

Which dyslipidemia class actually causes an increase in TG?

A

bile acid resins

28
Q

MOA of Plant Stenol Esters

A

-decrease cholesterol absorption, TC, and LDL

29
Q

What labs must be monitored for statin therapy?

A
  • baseline ALT
  • ALT as clinically indicated thereafter
  • CK prn myositis
30
Q

What labs must be monitored for fibric acid therapy?

A
  • baseline ALT and alk phos
  • ALT and alk phos 6-12 wks x2, then q12 mo thereafter
  • fasting lipid profile 6-12 wks after dose change, q12mo
  • CK prn myositis
31
Q

What labs must be monitored for bile acid resin therapy?

A

-fasting lipid profile 6-12 wks after stable dose then q12mo

32
Q

What labs must be monitored for nicotinic acid therapy?

A
  • baseline ALT and alk phos,
  • ALT and alk phos 6-12 wks, q12mo
  • after stable dose achieved x2 mos, fasting lipid profile, uric acid and glucose
  • fasting lipid profile q12 mo thereafter
  • CK prn myositis
33
Q

ACC/AHA Statin Benefit Groups

A
  • pts with clinical ASCVD
  • pts with LDL >190
  • pts 40-75 yo with DM and LDL 70-189 (but no clinical ASCVD)
  • pts w/o clinical ASCVD or DM with LDL 70-189 with 10 year risk of ASCVD >7.5%

Fall 2014 - Pharm Cardio (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions