Lipid Flashcards

1
Q

A major cause of coronary artery disease

A

atherosclerosis

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2
Q

CVD is a major cause of death in the US ____ people die each ehar from heart attacks, most commoly realted to ____

A

500,000

coronary artery disease

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3
Q

Atherosclerosis is characterized by

A

deposits of cholesterol and lipoproteins in artery walls. Three major classes of lipoproteins are found in the serum of fasting individuals

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4
Q

Three major classes of lipoproteins

A

low-density lipoproteins (LDL, “bad cholesterol”), high-density lipoproteins (HDL, “good cholesterol”), and very low-density lipoproteins (VLDL).

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5
Q

High concentrations of LDLs are associated with an increased risk of

A

CVD

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6
Q

Serum lipoproteins are formed via two pathways

A

dietary (exogenous) and liver synthesis (endogenous).

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7
Q

Exogenous pathway

A

involves absorption of lipids via intestine

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8
Q

Endogenous pathway

A

lipids originate from liver

Lipoproteins

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9
Q

Change in the lipid guidelines for 2018

A

. In this guideline there is no ideal target blood level of LDL, however, the guidelines do recognize that lower is better. The guideliens ustilize a isk calculator and has reocmmendations for primary prevention and secondary prevention

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10
Q

aims to prevent disease or injury before it ever occurs

A

Primary prevention

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11
Q

screening to identify diseases in the earliest. stages, before the onset of signs and symptoms, through measures such. as mammography and regular blood pressure testing

A

Secondary Prevention

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12
Q

Childhood screening - Risk factors

A

DM
Obesity
Family history of familial hypercholesterolemia

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13
Q

what should be emphasized with children

A

diet and exercise

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14
Q

Lifestyle Modifications

A

exercise 30 minutes a day

dietary therapy

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15
Q

dietary therapy recomendations

A

Reduced intake saturated fats not as strong
Consuming plant sterols (2 g/day)
Increased soluble fiber intake (10 to 25 g/day)
Dietary fiber of 20 to 30 g/day
Total calories to maintain or lose weight

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16
Q

3-hydroxyl-3-methyl-glutaryl-coenzyme A (HMG CoA) reductase inhibitors EXAMPLES

A

Lovastatin, pravastatin, simvastatin, fluvastatin, atorvastatin, rosuvastatin

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17
Q

Fibrates: fibric acid derivatives - EXAMPLES

A

Gemfibrozil, micronized fenofibrate, clofibrate

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18
Q

Bile acid sequestrants EXAMPLES

A

Cholestyramine, colestipol, colesevelam

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19
Q

Drug most effective in combination with statin

A

ezetimibe (Zetia)

20
Q

drug that has lost popularity

A

Niacin

21
Q

Vitamins/antioxidants/herbs/natural products

A

Vitamin E, vitamin C, folic acid, garlic, fish oils, fiber, coenzyme Q10, flaxseed

22
Q

Active liver disease is a contraindication for all treatments for hyperlipidemia except

A

bile acid sequestrants

23
Q

Statins MOA

A

Block synthesis of cholesterol in the liver by competitively inhibiting HMG CoA reductase activity

24
Q

Statins decrease levles of LDL by

A

25 to 65%

25
Q

Statins Modest decres in ___ and very modest increase in ___ may occur

A

Modest decreases in TGs (10% to 40%) and very modest increases in HDL (5% to 17%) may occur

26
Q

Statins preganacy

A

old category X; fully contraindicated

27
Q

All statins are metabolized a lease in part by _____ (except)

A

CYP3A

except fluvastatin and rosuvastatin

28
Q

CYP3A inhibitors may increase statin

A

concentrations.

Verapamil, diltiazem, azole antifungals, erythromycin, fluoxetine, nefazodone, protease inhibitors

29
Q

CYP3A inducers may (statin)

A

decrease statin concentrations.

Rifampin, phenytoin, phenobarbital

30
Q

Statins may also interact with other

A

CYP channel substrates; for example, cyclosporine

31
Q

Statin side effects

A

HA, myalgia, fatigue, GI intolerance, flu-like symptoms

32
Q

Statin Myopathy occurrence and avoidance

A

occurs in 0.2% to 0.4% of patients, some agents more likely
Reduced by using lowest effective dose
Cautiously combining statins with fibrates
Avoiding drug interactions

33
Q

Statins can have

A

myalgia (muscle aches)

34
Q

Active liver disease is a contraindication in

A

statins

35
Q

Active liver disease in statins occurs in

A

Occurs in 0.5% to 2.5% of cases and is dose-dependent.

Serious liver problems are rare.

36
Q

Liver side effects statin managment

A

reducing dose or stopping until levels return to normal.

37
Q

Clinical studies of statins have demonstrated a 0.5 to 3.0 percent occurrence of persistent elevations in aminotransferases in patients receiving

A

statins

38
Q

Statins start with

A

lower dose and increase, as needed, according to LDL response; absolute levels of LDL not as closely monitored now

39
Q

Rosuvastatin most potent - Dose

A

5 to 20 mg day

40
Q

Atorvastatin next most potent - Dose

A

10 mg/day initially, increase no fewer than 2 to 4 weeks

41
Q

What statin has the best ADR profile

A

Atorvastin

42
Q

Simvastain dose

A

20 to 40 mg/day

43
Q

Lovastatin (IR) 20 mg/day (XR) - Dose

A

40 to 60 mg a day

44
Q

Statin test liver function every

A

4 to 6 weeks then every 3 to 4 months until control established

45
Q

Statin liver function tests

A

before starting therapy and 3 to 6 months later only if suspected issues or underlying hepatic issues