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Pharmacology > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

Why lipoproteins are necessary

A

Triglycerides are an energy source. Cholesterol needed to make: cell membranes, bile acids, and steroid hormones

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2
Q

What is hyperlipidemia

A

Elevated cholesterol, triglycerides, and/or LDL

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3
Q

Physical exam signs of dyslipidemia

A

Xanthelasma (hands/eyes), circumferential Arcus, PVD (shiny, discolored, hairless), thickened Achilles, htn

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4
Q

Primary hyperlipidemia: what it is, also referred to as

A

Genetic/inherited heterozygous condition resulting in elevated total cholesterol or TG level. Familial

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5
Q

Primary HLD: numbers, need to get what

A

Total chol >200, tg >500. Thorough family hx

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6
Q

Secondary hyperlipidemia: from what 4 other conditions. Drugs that negatively impact/how: 3

A

DM, hypothyroid, chronic renal failure, obstructive liver disease. Inc LDL dec HDL: progestin, corticosteroids, anabolic steroids

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7
Q

If not fasting, which labs you can use

What indicates need to retest while fasting

A

Only total cholesterol and HDL.

TC >200 or HDL <40

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8
Q

Total cholesterol: desired, borderline, high

A

<200, 200-239, >240

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9
Q

HDL: low, high

A

<40. >60.

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10
Q

LDL:optimal, near optimal, borderline high, high, very high

A

O- <100. 100-129 near optimal. 130-159 borderline. 160-189 high. >190 v high

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11
Q

Old guidelines focused on what

A

Hyperlipidemia, assessment of ASCVD and tx of HLD to a goal LDL number

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12
Q

New guidelines focus on what

A

Reduction of ASCVD using statins based on evidence in RCTs

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13
Q

Screening: who and how often

A

20 years or older, every 4-6 years

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14
Q

What to screen: 8

A

Fasting lipoprotein: TC, LDL, HDL, TG. ALT, CK, hba1c. Estimated 10 yr ASCVD risk.

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15
Q

Primary prevention

A

Therapeutic lifestyle changes:rec for everyone. Reduce sat fats and cholesterol, inc activity, wt control

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16
Q

HDL
Elevated by 3
Lowered by 4

A

Elev: alcohol (1-2), sat fats, weight loss
Low: low fat diet, sugar, excess calories, excess polyunsaturated fats

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17
Q

LDL:
Elev by 3
Lowered by 3

A

Elev: sat fat, trans fatty acids, dietary cholesterol
Lowered: MUFAs, complex carbs, soy

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18
Q

Total cholesterol
Elev by: 2
Lowered by: 2

A

Elev: sat fats and transfatty acids
Low: substituting MUFAs and complex carbs for sat fats and lowered by soy

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19
Q

TGs
Elev by 4
Lowered by 2

A

Elev: alc, sugar, high carb diet, excess calories
Low: wt loss and fish oils

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20
Q

What % of calls should be sat fat

Total fat

A

Sat <7%. Total 25-35%

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21
Q

Areas to assess for cv disease

A

Coronary heart disease (angina, MI, PCI, stents, CABG)
PAD (carotid artery disease, extremities, abdominal AA)
Stroke/tia

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22
Q

RFs in ASCVD risk assessment

9

A

Gender, age, race, tc, HDL, SBP, tx for high bp, dm, smoker

23
Q

4 categories for statin therapy/secondary prevention ASCVD

Intensity of therapy depends on

A

Clinical ASCVD. LDL >190. DM. >7.5% estimated 10 yr risk. Depends on the category

24
Q

Statin therapy reduces risk for who
Moderate intensity does what
High intensity does what

A

Anyone with LDL >70
Moderate: 30-50% reduction LDL
High: >50% reduction LDL

25
Q

Statin therapy recommended for who

A

Anyone who would exp net benefit of ASCVD risk reduction over potential adverse effects

26
Q

High intensity statin therapy drugs 2

A

Atorvastatin 80 mg

Rosuvastatin 20 mg

27
Q

Moderate intensity statin therapy

A

Atorvastatin 40, rosuvastatin 10, simvastatin 20-40, pravastatin 40, love statin 40, fluvastatin 40, few others

28
Q

Low intensity statin therapy

A

Pravastatin 10-20, lovastation 20, 3 others

29
Q

Statins
Class
MOA

A

HMG COA reductase inhibitors. Inhibit the rate limiting enzyme in the formation of cholesterol. Decrease LDLs, decrease TGs, and increase HDLs

30
Q

Statin therapy
If <75
If >75

A

Is less than: high intensity therapy. If greater than or with contraindications to high intensity, should get moderate intensity statin

31
Q 
Statin tx for primary HLD 
LDL > \_\_\_ 
Reduction by \_\_\_ reduces risk by 20%
May require what 
Assess need to address what
A

>

  1. >
    1. Additional use of non statin lipid lowering agents to achieve acceptable lipid reduction. Hypertriglyceridemia.
32
Q

Diabetes
Benefits from statins
Which intensity

A

Substantial. Moderate is acceptable. High if 10 yr risk greater than 7.5%

33
Q

Ascvd risk assessment should be completed for who

A

Pts without ascvd or dm and ldl <190

34
Q

Non statin cholesterol therapy indic for who

A

High risk (ascvd, ldl >190, diabetes and 40-75) should take it if less than anticipated response to statins, unable to tolerate intensity, or are intolerant. Weigh benefits v risks and drug-drug

35
Q

Areas that need further research 4

A

Non HDL cholesterol/other biomarkers to guide tx, non invasive imaging to guide risk assessment, 10 yr risk assessment vs lifetime when age to begin statins, others: HF, ESRD on HD, HIV, transplant (groups that haven’t been researched)

36
Q

Secondary tx goals 2

A

Tx elev TGs: if >200 and ldl has been achieved, tx TGs

Tx low HDLs <40: if ldl and tg goals have been met, target HDL

37
Q

Bile acid sequestrants
MOA
3 ex

A

Bind bile acid in intestines, liver uses hepatic cholesterol to produce more bile acids. Effect is to decrease LDL and inc HDL. Questran, colestipol, colesevelam

38
Q

Nicotinic acid

MOA

A

Reduces production of VLDLs. Reduce LDLs, TGs, and inc HDLs

39
Q

Fibrin acid derivatives
MOA
Agents

A

Reduce synthesis and inc breakdown of VLDLs. Reduce LDLs and TGs and inc HDL. Gemfibrozil, fenofibrate, clofibrate

40
Q

Zeta
MOA
No effect on 2
Intended for use with

A

Inhibits cholesterol and phytosterol absorption from brush border of intestines. No effect on abs of vit ADEK, no effect on CYP450, use w a statin

41
Q

Zetia

Effect on LDL, other events

A

When added to simvastatin reduced LDL by 24% and reduces pt of cv death, coronary events, or nonfatal CVA

42
Q

Reduction of LDL by bile acid sequestrant

A

8-16% when used w statin

43
Q

Statin and fibric acid derivatives
Primarily used to what
Risk of
Contraindicated in

A

Decrease TGs. Risk myopathies. Dont use in severe liver disease

44
Q

Statin and niacin

Inc risk of

A

Hepatic dysfunction

45
Q

Lovastatin and simvastatin

Interact with which drugs: 6

A

Itraconazole, ketoconazole, erythromycin, clarithromycin, gemfibrozil, grapefruit juice

46
Q

Side effects statins
Major one
Occur with what
Indiv at risk: 4

A

Myopathies, occur w any statin. >80, small frame/frail, imp renal or hepatic system, alcohol abuse

47
Q

Myopathies w statins: drug combos w statins that inc risk 6

A

Niacin, gemfibrozil, cyclosporine, hiv protease inhibitors, verapamil, amiodarone

48
Q

Pregnant and nursing women should avoid which 4

One they can use

A

Dont use: statins, ezetimibe, niacin, fibric acid derivatives
Can use bile acid binding resins

49
Q

PCSK9 inhibitors

Benefit seen where

A

59% ldl reduction. Benefit seen across age, sex, and type of ASCVD regardless of starting LDL level

50
Q

Lopitamide

What it is

A

Tg transfer protein inhibitor, resides in ER and prevents assembly of Apob lipoproteins in enterocytes and hepatocytes. Inhib synth of chylomicrons and vldl in liver.

51
Q

What is no longer recommended, now what is the goal

A

No longer: tx to ldl or non HDL cholesterol. Now goal is intensity of statin therapy for ascvd reduction

52
Q

Focus should be assessing for what and If pts fall into which of 4 groups

A

Risk for ascvd. Clinical ascvd, ldl >189, indiv 40-75 w dm and ldl 70-189 w/o ascvd, indiv 40-75 with dm and ldl 70-189 and a 10 yr risk of 7.5% or higher

53
Q

Intensity of statin therapy based on 4

A

Presence of clinical ascvd, risk of developing ascvd, presence of dm w/without HLD, or presence of isolated hyperlipidemia (genetic)

Pharmacology (19 decks)

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