HLD Flashcards

1
Q

Hyperlipidemia

A

Increased cholesterol & triglycerides in the blood

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2
Q

Role of cholesterol

A

contributes to cell membrane permeability and function; essential for formation of bile acids, vitamin D, progesterone, estrogen, androgens, hormones

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3
Q

Where does cholesterol come from

A

MADE IN LIVER

some from diet

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4
Q

Funciton of lipoproteins

A

energy, storage, hormone production and bile acid; abnormal lipid metabolism leads to atherosclerosis (overproduction or receptor defect)

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5
Q

Types of lipoproteins

A
Chylomicrons
VLDL
IDL
LDL
HDL
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6
Q

Chylomicrons

A

carry dietary lipids from intestine to liver, skel. muscles and adipose tissue

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7
Q

VLDL

A

carry newly synthesized triglycerides from liver to adipose tissue

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8
Q

IDL

A

not usually detectable in blood

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9
Q

LDL

A

carry cholesterol from liver to body’s cells (BAD)

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10
Q

HDL

A

collect cholesterol from body tissue (vascular endo) and return it to liver; PROTECTIVE AGAINST HEART DISEASE

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11
Q

Lipid Metabolism

A
  1. Exogenous (diet, chylomicrons)
  2. endogenous (liver, VLDL, LDL, IDL)
  3. Reverse cholesterol transport (HDL)
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12
Q

Inherited lipid disorders

A

familial hypercholesterolemia
polygenic hypercholesterolemia
familial combined hyperlipidemia

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13
Q

Familial Hypercholesterolemia

A
monogenic
Rare 
Hetero: 2x LDL
Homo: 8 x LDL
Tx: Statin (+/- add on)
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14
Q

Polygenic hypercholesterolemia

A
presents similarly to familial hypercholesterolemia
multiple genes
increased LDL
premature onset of CHD
Tx: statin (+/- add on)
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15
Q

Familial combined hyperlipidemia

A

polygenic
50% of familial CHD
common (1-2% of population)
Tx: Statin (+/- add on)

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16
Q

What is more common, primary or secondary hyperlipidemia?

A

Inherited

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17
Q

Causes of secondary hyperlipidemia

A
DM
Excessive alcohol
Diet
Smoking
Obesity
Hypothyroidism
Chronic renal disease
Liver disease
Drugs
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18
Q

How atherosclerosis occurs:

A
  1. LDL molecules diffuse through endothelium at a rate dependent on concentration in blood
  2. Macrophages follow, absorb and become foam cells, then die & release cholesterol and form deposits
  3. Body reacts w/ increased collagen to form a cap
  4. Cap ruptures and thrombus forms leading to potential infarct
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19
Q

Screening for HLD

A

9-11 yo
17-21 yo
(earlier if high suspicion)

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20
Q

CHD non-modifiable risk factors

A
family hx
age (males >45, females >55)
male
symptomatic cardiovascular disease
chronic kidney disease
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21
Q

Modifable CHD Risk Factors

A
HTN (>140/90 or on antihypertensive)
DM
Tobacco use
Obesity
HLD or HDL <40
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22
Q

Negative risk favor for CHD

A

HDL >60 (GOOD!!!)

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23
Q

Testing for HLD

A

Fasting lipid Panel (chol, tirglycerides, LDL and HDL) - 12 hour fast (triglycerides greatly affected by eating; acutely ill patients may have falsely low chol levels)

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24
Q

Cholesterol Range

A

Desirable: < 200 mg/dl
Borderline: 200-238 mg/dl
High: 240 mg/dl

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25
Q

Triglyceride Range

A

Desirable: <150 mg/dl
Borderline: 150-199 mg/dl
High risk: 200-499 mg/dl

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26
Q

HDL Range

A

Desirable: 60 mg/dl
Borderline: 35-45 mg/dl
High risk: <35 mg/dl

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27
Q

LDL Range

A

Desirable: 60-130 mg/dl
Borderline: 130-159 mg/dl
High risk: 160-189 mg/dl

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28
Q

Cholesterol-filled, soft, yellow plaques that indicated familial or secondary HLD

A

plane xanthomas

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29
Q

Tuberous xanthoma

A

yellow-orange nodules over knees and elbows, can also be in tendons (tendinous xanthoma);

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30
Q

What is tuberous xanthoma associated with?

A

Familial hypercholestolemia (monogenic)

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31
Q

Eruptive Xanthomas

A

small red-yellow papules w/ abrupt onset;
extensor surfaces and buttocks
Caused by elevated triglycerides >1500 mg/dl
Indicates Familial HLD

32
Q

Sign of familial HLD

A

Tuberous xanthoma & eruptive xanthomas

33
Q

Corneal Arcus

A

gray ring around the cornea

Abnormal <40 yo

34
Q

DASH diet (Dietary Approaches to Stop Hypertension)

A
fruits and veggies
moderate in low-fat dairy
low in animal protein
contains plant protein
low sodium
(decreases BP, LDL and risk of CHD and stroke)
35
Q

Tx for HLD

A

Diet
Exercise (3-4 sessions/week each 40 min) (INCREASES HDL)
Meds (statins, fibrates, nicotinic acid, bile acid sequestrants, cholesterol absorption inhibitors, PCS9 inhibitors)

36
Q

Statins

A

Dec. incidence of major vascular events

STABILIZE VULNERABLE PLAQUES AND REDUCE THE UNDERLYING INFLAMMATION

37
Q

MOA of Statins

A

Inhibit HMG-CoA reductase (cholesterol synthesis in liver)

  • less cholesterol produced so blood cholesterol decreases
  • liver enzymes increase production of LDL receptors which bind circulating LDL more readily and digest LDL
38
Q

Effects of statins

A

lower LDL 20-60%

Lower triglycerides 15-30%

39
Q

Adverse effects of statins

A
mild GI
liver toxicity
myalgias, myositis, myopathy
rhabdo
GIVE AT BEDTIME (when more cholesterol is being produced)
40
Q

Contraindications for statins

A

Absolute: active liver disease, pregnancy

Caution: concomitant use of CYP3A4 drugs, chronic kidney/liver disease

41
Q

Monitoring Statin therapy

A

baseline lipid panel, LFT, CK should be obtained
Repease lipid panel 6-8 weeks after statin tx. begins
Then assessment every 6-12 months

42
Q

Resin (bile acid sequestrants)

A

bind bile acids in the intestine and prevent reuptake
decrease LDL up to 24%
synergistic w/ statins
SAFE IN PREGNANCY

43
Q

Types of resins

A

cholestyramine, colesevelam, colestipol

44
Q

Adverse effects of resins

A
constipation
gas
interfere w/ fat soluble vitamin absorption
effect warfarin
CAN INCREASE TRIGLYCERIDES
45
Q

Contraindications for resins

A

Absolute: TGs >400 mg/dl
Relative: triglycerides >200 mg/dL

46
Q

Nicotinic acid (Niacin)

A

Reduce production of LDL
INCREASES HDL
may reduce triglycerides

47
Q

Adverse effects of nicotinic acid

A

flushing and pruritus
LIVER DAMAGE, monitor LFTs (more toxic than statins)
safety concern when used with statin!

48
Q

Don’t use with statin

A

nicotinic acid

49
Q

Contraindications of nicotinic acid

A

Absolute: active liver disease
Relative: hyperuricemia, hyperglycemia, unstable angina, NOT USED IN PREGNANCY

50
Q

Safe in pregnancy

A

bile acid sequestrants (resins)

51
Q

Fibric acid derivatives drugs

A

gefibrozil, fenofibrate, bezafibrate (all FIB)

52
Q

Use for fibric acid derivatives

A

LOWERING TRIGLYCERIDES (50%)
raising HDL (up to 25%)
USE IN THOSE WITH ELEVATED TG
not used in pregnancy!

53
Q

Adverse effects of fibric acid derivatives

A

gallstones
hepatitis
myositis

54
Q

Contraindications of fibric acid derivatives

A

absolute: severe hepatic or renal disease, preexisting gallstones, taking SIMVASTATIN

Relative: other statin use (myopathy risk), concurrent warfarin use

55
Q

Ezetimibe MOA

A

blocks intestinal absorption of dietary and biliary cholesterol via transporter

56
Q

Ezetimibe role

A

can lower LDL

CAN BE USED CONCOMITANTLY W/ STATIN

57
Q

contraindications for ezetimibe

A

use w/ statin in active liver disease, pregnancy

58
Q

PCSK9 Inhibitors

A

proprotein convertase subtilisin kexin 9; protease produced in liver causes increased LDL levels; inhibiting this reduces LDL levels by 70%
Expensive
Requires INJECTIONS

59
Q

Raises HDL

A

Niacin

60
Q

Safe in pregnancy

A

Resins

61
Q

Statin add-on

A

Ezetamibe (except in liver disease)

62
Q

4 Statin Benefit Groups

A
  1. Clinical ASCVD
  2. LDL >190 mg/dL
  3. DM (40-75 yo) w/ LDL 70-189 mg/dl without clinical ASCVD
  4. W/o ASVD or DM with LDL 90-189 mg/dL and estimated 10 year risk >7.5%
63
Q

What constitutes clinical ASCVD?

A

Acute coronary syndromes
Hx of MI
stable/unstable angina
stroke or TIA

64
Q

Clinical ASCVD tx

A

<75 yo: high intensity

>75 yo: moderate

65
Q

LDL-C >190

A

high intensity statin (moderate if not candidate)

66
Q

DM (40-75)

A

moderate intensity statin

Risk >7.5%: high intensity statin

67
Q

Risk >7.5%

A

moderate to high risk statin

68
Q

High cholesterol

A

> 240

69
Q

High TG

A

> 200

70
Q

Highrisk HDL

A

<35

71
Q

LDL highrisk

A

160-189

72
Q

Normal cholesterol

A

<200

73
Q

Normal TG

A

<150

74
Q

Normal HDL

A

60

75
Q

Normal LDL

A

60-130