Treatment of Dyslipidemia Flashcards

1
Q

Steps to evaluating dyslipidemia

A
  1. Fasting Lipid Profile
  2. Rule out secondary causes
  3. CHD Risk equivalents
  4. Major CHD Risk Factors
  5. Estimate 10 year risk with Framingham Score
  6. Establish treatment goals and therapy based on risk category
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2
Q

For what population is a lipid screening appropriate for?

A

All adults aged 20 or over, every 5 years

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3
Q

Secondary causes of Dyslipidemia

A
  • Diabetes
  • Hypothyroidism
  • Obstructive liver disease
  • Chronic renal failure
  • Drugs that can increase LDL, decrease HDL (prostaglandins, thiazide diuretics, beta blockers, isotretinoin)
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4
Q

CHD Risk Equivalents

A

DM

peripheral arterial disease

abdominal aortic aneurysm

symptomatic carotid artery disease

multiple RF’s that confer a 10 year risk >20%

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5
Q

Major CHD RIsk Factors

A
  • current smoker
  • HTN >140/90 or on antihypertensive
  • Low HDL <40
  • FHx of premature CHD (55/65 MI or sudden death)
  • Age and gender (45/55)
  • Negative point: HDL >60

**If two or more risk factors are present, assess 10 year CHD risk

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6
Q

Therapeutic Lifestyle Changes

A

Healthy diet

Weight reduction

Increased physical activity

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7
Q

Metabolic syndrome

A

Three or more of:

Abdominal obesity

High TG

Low HDL

High BP

Insulin resistance

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8
Q

More common name of HMG Co A Reductase Inhibitors

A

statins

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9
Q

Statin mechanism of action

A

inhibit HMG CoA Reductase, thereby blocking endogenous cholesterol synthesis

stimulate hepatic LDL receptors, enhancing LDL clearance from plasma

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10
Q

Adverse effects of statins

A

Hepatic toxicity

Myopathy

Neuropathy

Reversible cognitive side effects

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11
Q

Contraindications of statins

A

pregnancy category X

active or chronic liver disease

Relative CI: niacin or gemfibrozil concomitant use

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12
Q

Statins have what kind of dosing curve do statins have?

A

Non linear–after a certain amount, little effect is had by doublin doses

Works best when dose at night

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13
Q

Bile Acid Resins (BAR)

Mechanism of action

A

Bind bile acids, forming an insoluble complex that is eliminated in the stool.

This promotes conversion of cholesterol to BAs in the liver.

May increase hepatic VLDL, increasing TGs

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14
Q

Adverse effects of Bile Acid Resins

A

GI symptoms–constipation, belching, flatulence, heart burn, abdominal distention nausea

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15
Q

CI of Bile Acid Resins

A

High TGs

H/O severe constipation

Decreases the absorption of other meds so stagger

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16
Q

Reasons to use BAR

A

Good in young pts with moderately high LDL, or in combination of statins for severe hyperlipidemia

Can be used with niacin and fibric acids

17
Q

Fibric Acids mechanism of action

A

Increase lipoprotein lipase activity, enhacing VLDL and IDL catabolism, decreasing TGs

Promotes secretion of cholesterol in bile

18
Q

Adverse effects of fibric acids

A

GI complaints

Increase bile lithogenicity

19
Q

When to use fibric acids

A

Very good at lower TGs

Good for combined dyslipidemia

Avoid with statins (increase myositis)

20
Q

Nicotinic Acid mechanism of action

A

Inhibits synthesis of VLDLs, lowering LDLs

21
Q

Adverse effects of nicotinic acid

A

Flushing (MC)

May cause glucose intolerance and increase uric acid

Older forms cause hepatitis

22
Q

CI of nicotinic acid

A

Liver disease

DM

gout

hyperuricemia

23
Q

When to use nicotinic acid

A

Good for mixed hyperlipidemias

Start low, go slow, montitor for hepatic toxicity

Can take with aspirin to dec flushing

24
Q

Cholesterol absorption inhibitors (ezetimibe) mechanism of action

A

Selectively inhibits the absorption of cholesterol

25
Q

Adverse effects of cholesterol absorption inhibitors (ezetimibe)

A

fatigue,

abdominal pain

HA

diarrhea

arthralgia

26
Q

When to use cholesterol absorption inhibitors (ezetimibe)

A

Can use in conjunction with statins if not reaching goal

27
Q

Supplements for lowering cholesterol

A

Plant stanol esters: dec cholesterol absorption

Fish oils: esp if need lower TGs

Blond psyllium

Oat bran