Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm N895 > Antihyperlipidemics > Flashcards

Antihyperlipidemics Flashcards

(69 cards)

Start Studying
1
Q

Types of lipids

A

Low density lipoproteins (LDL)

Very low density lipoproteins (VLDL)

Triglycerides (TG)

High density lipoproteins (HDL)

emerging data on additional lipoproteins

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

LDL and lipid lowering therapy

A

“bad” cholesterol & primary target of lipid lowering Tx

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

CV risk and LDL

A

CV risk increases w/increasing LDL

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

Origin and role of VLDL

A

secreted by liver, some are converted to LDL

Export TGs to peripheral tissues

tend to see w/ingestion of excessive calories

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

TGs: what is hypertriglyceridemia associated with?

A

pancreatitis

pancreatitis typically at very high levels, e.g., >500mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why is a fasting lipid panel recommended?

A

TGs increase after food–

new evidence shows may not change >10%, so not so important

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Drugs that may induce hypertriglyceridemia

A

TPN, propofol, cleviprex (clevidipine), protease inhibitors, alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

HDL and lipid therapy

A

“good” cholesterol & secondary target for dyslipidemia

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

HDL and CV risk

A

declines w/higher HDL

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

Secondary causes of elevated LDL and TG

A

Diet, medications, comorbid conditions, disordered/altered metabolism

altered metabolism is most common

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

ATP III Guidelines: Total cholesterol (mg/dL)

Optimal/desirable, near optimal, borderline high, high

A
  • Optimal/desirable: <200
  • borderline high: 200-239
  • high: > 240
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ATP III Guidelines: LDL cholesterol (mg/dL)

Optimal/desirable, near optimal, borderline high, high

A
  • Optimal/desirable: <100
  • near optimal: <100-129
  • borderline high: 130-159
  • high: 160-189
  • very high: _>_190
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ATP III Guidelines: TGs (mg/dL)

Optimal/desirable, borderline high, high

A
  • Optimal/desirable: <150
  • near optimal
  • borderline high: 150-199
  • high: >/=200
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ATP III Guidelines: HDL Cholesterol (mg/dL)

Optimal/desirable, near optimal

A
  • Optimal/desirable: >/=60
  • near optimal: >40 men, >50 women
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ATP III Guidelines

A

Former guidelines based on risk factors

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

Niacin + statin

A

previously what we did but no added benefit so no longer rec’d to combine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

2013 ACC/AHA Guidelines

A
  • Replaced ATP III
  • no longer to Tx LDL chol targets
  • Non statin therpay discouraged in most cases
  • Lifestyle modification rec’d for all pts
  • 10yr ASCVD risk calculator - risk category determines what level of statin therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Statins: when risk may outweigh benefit / C/Is / avoid in…

A
  • Risk > benefit: NYHA class II-IV HF; Maintenance hemodialysis; LDL-C <70mg/dL
  • **Avoid in: **severe hepatic impairment
  • **C/I: **pregnancy & lactation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Initial evaluation: labs

A
  • Fasting lipid panel: to assess adherence and predicted response
  • ALT
  • CK
  • HbA1c
  • Hx of prior or current muscle Sx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Evaluation: lipid panel

A
  • LDL-D >190mg/dL should assess for secondary cause or screen family for familial hyperlipidemia
  • TG: >500mg/dL should be treated
  • Repeat 4-12 w, then q3-12mths when response established
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Evaluation: significance of ALT

A

result >3x ULN is C/I to statin therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pharmacologic therapy for dyslipidemia

A
  • HMG-CoA reductase inhibitors (statins)
  • fibrates
  • bile acid sequestrants
  • sterol absorption inhibitor
  • nicotinic acid
  • omega3 ethyl esters
  • plant sterols/stanols
  • red yeast chinese rice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Statins: Agents

A

Lovastatin/Mevacor

Pravastatin/Pravachol

Simvastatin/Zocor

Fluvastatin/Lescol XL

*Atorvastatin/Liptor

*Rosuvastatin/ Crestor

*can be dosed High intensity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Statins: MOA

A

Inhibits HMG-CoA reductase from converting HMG-CoA to cholesterol,

thereby reducing cholesterol synthesis.

Up-regulates LDL receptors on hepatocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Statins: Adverse Effects
rare confusional state or memory impairment, hepatic dysfunction, myopathy, rhabdomyolysis, DM, hemorrhagic stroke
26
Statins: timing of dose
some agents more effective when given in evening when most chol synthesis occurs
27
Who is at highest risk for AEs from statins?
multiple comorbidities including renal or hepatic impairment; Hx statin intolerance or muscle d/os; unexplained ALT \>3x ULN; Age \>75y; genetic polymorphisms or concomitant drugs that decrease statin metabolism/clearance
28
Statins: what to do if muscle sx
D/C statin. Evaluate factors that may predispose pt to Sx. R/O other causes Next steps diff depending on severe vs mild/mod
29
what to check in severe muscle sx
Check CK, Cr, urinalysis for myoglobinuria
30
What to do if mild-moderate sx on statin, after d/cing dose
* Resolve & no C/Is --\> restart same statin at same or lower dose * Resolve, statin established as cause --\> use low dose of diff statin then increase as tolerated * Sx unresolved after 2mth --\> consider other causes. If other cause identified, restart original statin at original dose
31
Statins: CYP3A4 substrates
Lipitor (atorvastatin) Zocor (simvastatin) Mevacor (lovastatin)
32
Statins: CYP2C9
Crestor (rosuvastatin) - substrate Lescol XL (fluvastatin) - inhibitor
33
Statins: which one reduce in renal impairment
Crestor (rosuvastatin)
34
Statin w/low potential for drug interactions, low potency (not necessarily low intensity)
Pravachol (pravastatin)
35
Anticipated response of High, moderate, low intensity
High: \>/= 50% Moderate: 30-50% Low: \<30% (not recommended)
36
Which statin has increased myopathy at 80mg/day?
Zocor (simvastatin)
37
Fibrates: MOA
peroxisome proliferator-activated receptor alpha agonists, reduced secretion of VLDL, increased lipoprotein lipase activity, increase HDL (mainly to lower TGs)
38
FIbrates: ADRs
dyspepsia, rash, hypokalemia, myopathy, hepatic dysfunction, gallstones, rare blood dyscrasias, rhabdo
39
Fibrates: caution in what populations & why?
obese, females, Native Americans due to increased risk of gallstones
40
Fibrates: renal / hepatic
Avoid in renal or hepatic impairment
41
Concomitant therapy w/statins and fibrates
Avoid! Increased risk myopathy and rhabdo \*may consider adding fenofibrate to a low or moderate intensity statin in select cases if benefits \> risks (e.g., TG \>500mg/dL)
42
Fibrates: Agents
lopid (gemfibrozil), tricor (fenofibrate)
43
Fibrates and CYPs
Lopid (gemfibrozil) is CYP2C9 and CYP2C19 inhibitor
44
Zetia (ezetimibe): MOA
sterol absorption inhibitor, in bile inhibits resorption of chol, decreases LDL
45
Zetia (ezetimibe): ADRs
rare hepatic dysfunction, myositis
46
Zetia (ezetimibe): Monitoring
baseline LFTs, discontinue if persistent ALT \>3x ULN
47
Zetia (ezetimibe): how are they used?
generally in combo w/HMG-CoA reductase inhibitors (statins)
48
Zetia (ezetimibe): contraindications
pregnancy and lactation
49
Bile Acid Sequestrants: MOA
Prevent reabsorption of bile acis by binding them in the intestinal lumen, increased chol catabolism, upregulate LDL receptors
50
Bile acid sequestrants: AEs
constipation, bloating, heartburn, diarrhea, increased VLDL
51
Bile acid sequestrants: monitoring
fasting lipid panel at baseine, 3mths, then every 6-12mths
52
Bile acid sequestrants: avoid in
diverticulitis, TG \>/= 250mg/dL (**C/I \>400), **type III hyperlipoproteinemia
53
Bile acid sequestrants:​ effect on nutrient absorption
may impair vit K and FA absorption must take with food to be effective
54
Bile acid sequestrants and drug interaction
administer other meds 1 hour prior, or 2 hours after to limit interaction
55
Bile acid sequestrants:​ Agents
Colestid (colestipol) questran (cholestyramine) Welchol (colesevelam)
56
Niaspan (nicotinic acid): what is it?
Vit B3
57
Niaspan (nicotinic acid): MOA
reduced VLDL hepatic secretion and catabolism of apoAl; increased HDL, reduced LDL and TG
58
Niaspan (nicotinic acid): dosing
initiate at low dose, then titrate as tolerated over weeks
59
Niaspan (nicotinic acid): Monitoring
fasting BG or HbA1c, LFTs, uric acid at baseline, when dose increase and Q6mths
60
Niaspan (nicotinic acid): how to prevent flushing
pre-medication w/aspirin 325mg 30min prior to nicotinic acid dose
61
Niaspan (nicotinic acid): contraindications
pregnancy and lactation
62
Niaspan (nicotinic acid): ADRs
flushing, pruritis, rash, dry skin, nausea, abdominal discomfort, hyperuricemia, rare hepatotoxicity, arrhythmias, macular edema
63
Niaspan (nicotinic acid): discontinue niacin if...
persistent severe cutaneous symptoms, persistent hyperglycemia, acute gout, unexplained abdominal pain or GI Sx, new onset afib, new onset weight loss
64
Omega-3 Ethyl Esters: available forms
Lovaza by prescription or over-the-counter fish oil capsules; 3-4gm docosahexaenoic and eicosapentaenoic acids/day
65
Omega-3 Ethyl Esters: MOA
reduce hepatic synthesis of TGs, increase plasma lipoprotein lipase activity
66
Omega-3 Ethyl Esters:​ Adverse Effects
pruritis, rash, dysgeusia, dyspepsia, constipation, LFT abnormalities, may increase LDL levels
67
Omega-3 Ethyl Esters:​ monitoring
GI disturbances, skin changes, bleeding
68
When to consider Omega-3 Ethyl Esters?
may consider when TG \>500mg/dL
69

Pharm N895 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions