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X Clin Med II Exam 1 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

What is the function of lipoproteins?

A

Because lipids are insoluble in plasma, circulating lipids are carried in these
Used for energy, storage, hormone production and bile acid formation

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2
Q

What happens after abnormal lipoprotein metabolism?

A

Atherosclerosis (usually genetic because of defective receptors so there is overproduction/impaired removal of lipoproteins)

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3
Q

What are the 5 types of lipoproteins?

A

Chylomicrons, VLDL, IDL, LDL and HDL

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4
Q

Function of chylomicrons

A

Carry dietary lipids from intestine to liver, skeletal muscle and adipose tissue

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5
Q

Function of VLDLs

A

Carry newly synthesized triglycerides from liver to adipose tissue

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6
Q

Function of IDLs

A

Intermediate between VLDL and LDL (usually not detectable in blood)

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7
Q

Function of LDLs

A

Carry cholesterol from liver to body’s cells

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8
Q

Function of HDLs

A

Collect excess cholesterol from body’s tissues (including vascular endothelium) and return it to the liver
Basically reverse cholesterol transport to provide protection against heart disease

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9
Q

What do you want to suspect in anyone with a family history of premature atherosclerotic cardiovascular disease?

A

An inherited increased lipid disorder (familial hypercholesterolemia, polygenic hypercholesterolemia or familial combined hyperlipidemia)

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10
Q

What is familial hypercholesterolemia?

A

Monogenic and very rare
Homozygotes have much more LDL than heterozygotes
Treat with a statin (and maybe add on)

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11
Q

What is polygenic hypercholesterolemia?

A

Very similar to familial but multiple genes!
Increased LDL with premature onset of CHD
Treat with a statin (and maybe add on)

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12
Q

What is familial combined hyperlipidemia?

A

Polygenic with a wide variety of lipid abnormalities
Present in almost half of people with familial CHD
Treat with a statin (and maybe add on)

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13
Q

What is secondary hyperlipidemia?

A

Etiology that does not relate to lipid metabolism (diabetes and excessive alcohol most common, also obesity, smoking, renal/liver disease, drugs etc)

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14
Q

Process of atherosclerosis

A

LDLs diffuse through endothelium at a rate that is dependent on the concentration in the blood!
Macrophages follow, absorb them, become foam cells and then die to release cholesterol and form deposits
Body reacts with increased collagen to form a cap
Cap ruptures and thrombus forms leading to a potential infarct

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15
Q

When is it recommended to screen?

A

Between 9-11 and again at 17-21 yrs

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16
Q

Non-modifiable risk factors of CHD

A 
Family history of premature ASCVD
Age (male over 45 and female over 55)
Male
Symptomatic cardiovascular disease (angina etc)
Chronic kidney disease
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17
Q

Modifiable risk factors of CHD

A 
HTN (BP over 140/90 or on antihypertensive)
DM
Smoking
Obesity
Hyperlipidemia or HDL<40
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18
Q

What is a negative risk factor of CHD?

A

HDL > 60

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19
Q

What is on a fasting lipid panel?

A

Total cholesterol, triglycerides, LDL and HDL

Total cholesterol= HDL + LDL + (TAGs/5)

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20
Q

Why do you need to 12 hour fast before a fasting lipid panel?

A

Cholesterol isn’t really affected by eating but TAGs are and they are done at the same time

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21
Q

Cholesterol levels and acute MI

A

Levels can drop 24-48 hrs after acute MI and can persist up to 60 days

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22
Q

Lipid profile cutoffs

A

Cholesterol: <200 mg/dL good, 240 high risk
TAGs: <150 good, 200-499 high risk
HDL: 60 good, <35 high risk
LDL: 60-130 good, 160-189 high risk

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23
Q

What are plane xanthomas?

A

Cholesterol-filled, soft, yellow plaques that appear in various places (can indicate familial or secondary causes)

24
Q

What are tuberous xanthomas?

A

Yellow-orange nodules often over knees and elbows (can also be in tendons)
Associate with familial hypercholesterolemia

25
Q

What are eruptive xanthomas?

A

Crops of small red-yellow papules with ABRUPT ONSET
Seen on extensor surfaces and butt
Caused by elevated TAGs >1500 (indicate familial HLD

26
Q

What is corneal arcus?

A

White or grey ring around the cornea

Abnormal in pts under 40!

27
Q

What is the approach to lipid management?

A

Diet, exercise and meds

28
Q

DASH diet

A

For HTN/hyperlipidemia
Rich in fruits and veggies, moderate low fat dairy, low animal protein, plant sources of protein, low sodium
Goal is to decrease BP, LDL and hopefully decrease risk of CHD and stroke

29
Q

What can increase HDL cholesterol?

A

Exercise

30
Q

Types of medications used

A 
HMG Co-A reductase inhibitors (statins)
Fibrates
Nicotinic acid
Bile acid sequestrants
Cholesterol absorption inhibitors
PCSK9 inhibitors
31
Q

Why are statins used?

A

To decrease incidence of major vascular events and coronary mortality
Think they stabilize vulnerable plaques and reduce inflammation

32
Q

How do statins work?

A

Inhibit HMG-CoA reductase (rate limiting step in cholesterol synthesis in liver)
Less cholesterol is produced to decrease blood levels
Liver enzymes sense this and increase LDL receptors
Relocate to membrane and bind LDL and VLDL to take more cholesterol out of blood
LDL and VLDL goes to liver and gets digested

33
Q

Lipid panel changes with a statin

A

Lower LDL by 20-60%

Lower TAGs by 15-30%

34
Q

Adverse effects of statins

A

Mild GI, liver toxicity, myalgia, myositis, myopathy, rhabdo

35
Q

Contraindications of statins

A

Absolute: Active liver disease and pregnancy
Caution: use of other CYP3A4 inhibitors and various drugs, chronic kidney/liver disease

36
Q

What baseline should you obtain before statin therapy?

A

Lipid panel, LFTs and creatine kinase levels

37
Q

What should you consider when there is a poor response or intolerance to statin therapy?

A

Reinforce adherence to meds and lifestyle changes
Exclude secondary causes
Investigate statin intolerance

38
Q

When should the addition of a nonstatin LDL lowering agent be considered?

A

In ppl at high ASCVD risk that are getting the maximum tolerated statin and there is an insufficient response

39
Q

What are bile acid sequestrants (resins)?

A

Ex: cholestyramine, colesevelam, colestipol
Bind bile acids in the intestine to inhibit their absorption
Decrease LDL by up to 24%
Act synergistically with statins
Safe in pregnancy!

40
Q

Adverse effects of resins

A

Constipation, gas, may interfere with fat soluble vitamin absorption, affect warfarin management, increase TAGs

41
Q

Contraindications of resins

A

Absolute: TAGs >400
Relative: TAGs >200

42
Q

What does nicotinic acid do?

A

Reduce production of LDL, increase HDL and may reduce TAGs

43
Q

Adverse effects of nicotinic acid

A

Flushing and pruritus, liver damage, safety concerns when combo with statin

44
Q

Contraindications of nicotinic acid

A

Absolute: active liver disease
Relative: hyperuricemia, hyperglycemia, unstable angina
Don’t use in pregnancy

45
Q

What do fibric acid derivatives do?

A

(Gemfibrozil, fenofibrate, bezafibrate)
Mostly lower TAGs, raise HDL
Don’t usually use in pregnancy

46
Q

Adverse effects of fibric acid derivatives

A

May induce gall stones, hepatitis and myositis

47
Q

Contraindications of fibric acid derivatives

A

Absolute: severe hepatic or renal disease, preexisting gallstones, taking simvastatin
Relative: other statin use (risk of myopathy), concurrent warfarin use

48
Q

What does Ezetimibe do?

A

Blocks intestinal absorption of dietary and biliary cholesterol via transporter
Lower LDL up to 17%
Can use with statin
Contra: do not use with statin in active liver disease and pregnancy

49
Q

PCSK9 inhibitors

A

(Evolocumab, alirocumab)

Limited experience and data but should reduce LDL levels

50
Q

What are the 4 statin benefit groups?

A

Individuals with clinical ASCVD (acute coronary syndromes, history of MI, stable or unstable angina)
Individuals with LDL>190
Individuals with diabetes aged 40-75 yrs with LDL 70-189 and without clinical ASCVD
Individuals without ASCVD or diabetes with LDL 70-189 and estimated 10 yr ASCVD risk is >7.5%

51
Q

What statin level is used for people with clinical ASCVD?

A

Less than 75: high intensity

Over 75: moderate intensity

52
Q

What statin level is used for group 2?

A

High intensity

53
Q

What statin level is used for group 3?

A

Moderate intensity (high when 10 yr wisk is over 7.5%)

54
Q

What statin level is used for group 4?

A

Moderate to high

55
Q

What is the biggest contributor to ASCVD risk calculator?

A

Age

56
Q

What factors can also be used to initiate stain therapy if not in the 4 groups?

A

LDL >160, family history of premature ASCVD, Hs-CRP>2 mg/L, ABI

X Clin Med II Exam 1 (7 decks)

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