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Foundations > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Hyperlipidemia

A

Elevated TG & total cholesterol

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2
Q

Cholesterol forms what?

A

Forms steroid hormones/bile acids.

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3
Q

Triglyceride function

A

Transfers energy from food to cells.

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4
Q

Lipoproteins

A

Transfer lipids via apoproteins.
Low density: High TG.
High density: High apoproteins.

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5
Q

Two types of lipids

A

Cholesterol & TG

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6
Q

VLDL physio/pathway

A
  1. Made in liver
  2. VLDL transfers TG to cells
  3. Turns into LDL.
  4. LDL transfers cholesterol to cells
  5. Excess taken by liver & excreted via bile
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7
Q

HDL physio/path

A

Made in liver & intestine.

Collects LDL from plaques & cells and transfers to liver.

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8
Q

CVD (Cardiovascular disease/ASCVD)

A

CHD, Cerebrovascular, Peripheral artery, aortic atherosclerosis, AAA, TAA.

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9
Q

Primary HLD

A

Genetic abnormality due to cholesterol metabolism

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10
Q

Secondary HLD

A

Due to: DM, Alcohol, Renal ds, Cholestatic liver ds, Meds, Obesity/diet/sedentary

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11
Q

Medications causing secondary HLD

A
  1. OCP
  2. Thiazide diuretics
  3. Beta-blockers
  4. Atypical antipsychotics
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12
Q

Components measured

A

Total cholesterol & HDL

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13
Q

VLDL calculation

A

(TG/5)

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14
Q

LDL calculation

A

Total cholesterol-HDL-(TG/5)

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15
Q

LDL estimation incorrect if…

A

TG are above 200

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16
Q

Causes of abnormal cholesterol metabolism

A
  1. Genetic
  2. Insulin Resistance
  3. Organ dysfunction
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17
Q

Plaque formation

A
  1. LDL sticks to artery wall
  2. LDL oxidized (Pro-inflammatory & thrombotic)
  3. Macrophages eat lipids= Foam cells
  4. Endothelial dysfunction
  5. Vasoconstriction leads to exertional angina
  6. Plaque ruptures leads to MI/TIA/CVA
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18
Q

Non-modifiable risk factors

A
  1. M>45, F>55
  2. Male
  3. Premature family hx
    (M<55, F<65, 1st degree)
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19
Q

Modifiable risk factors

A
  1. Dyslipidemia, Low HDL,
  2. HTN
  3. Alcohol/smoking/diet
  4. DM
  5. PAD
  6. Renal ds
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20
Q

Under 65, what % dx/death

A
  1. Dx: 50%

2. Death: 15%

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21
Q

Hard Coronary Framingham risk

A

10 year risk of MI/death

Takes into account: Age, sex, smoke, Cholesterol, HDL, SBP, Tx.

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22
Q

ACC/AHA risk score

A

10 year risk of Heart disease/stroke

Takes into account: same + Race, DBP, Diabetes

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23
Q

High LDL/HDL relationship with ASCVD

A

High LDL high ASCVD
Decrease 1% LDL, Decrease CVD 1-1.5%
High HDL low ASCVD
Increase 2-3% HDL, Decrease CVD 2-4%

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24
Q

Primary vs Secondary prevention

A

Primary: modest benefits
Secondary: Strong benefits (if already had event)

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25
Q

Physical exam signs

A

Xanthomatous tendons (Plaques on knuckles/elbows)
Xanthelasma (plaques on eyelids)
Corneal arcus
Lipemia retinalis (white arteries on retina)
Eruptive xanthomas

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26
Q

NCEP ATP III 9 steps

A
  1. Fasting lipid panel
  2. CHD risk equivalent
  3. Major risk factors
  4. Framingham risk (if 2+ rf/CHD equiv)
    >20%=CHD risk equivalent
  5. Determine LDL goal dependent on risk category
    6.TLC
  6. Drug therapy for LDL
  7. Metabolic syndrome after 3 mo (ID&treat)
  8. Treat TG/HDL
27
Q

Optimal fasting levels

A
  1. Total: less than 200
  2. LDL: less than 70
  3. HDL: greater than 40, greater than 50 for women
28
Q

CHD equivalent

A
  1. Coronary artery disease
  2. Peripheral artery disease
  3. AAA
  4. Diabetes
29
Q

Major risk factors

A
  1. Smoking
  2. HTN
  3. HDL <40
  4. Family hx premature CAD
  5. Men>45, Women>55
30
Q

LDL goals for categories

A
  1. CHD/Equivalent: <70
  2. 2+ risk factors: <100
  3. 0-1 risk factors: <160
31
Q

TLC & effect on LDL

A
  1. Low fat diet (<30% calories)
  2. Cholesterol <200 daily
  3. Increase viscous fiber (10-25g)
  4. Plant stanols/sterols
  5. Weight management

Decrease LDL 25-30%

32
Q

When to initiate drug therapy?

A

After 3 months of TLC, LDL still high

33
Q

Metabolic syndrome (3 of 5)

A
  1. Abdominal obesity (40M, 35W)
  2. TG > 150
  3. Low HDL
  4. Elevated BP
  5. Fasting glucose >100
34
Q

TG values

A
  1. Normal: <150
  2. Mild hypertrig: 200-499
  3. Moderate/Risk for pancreatitis: >500
  4. Large risk for pancreatitis: >1000
35
Q

ACC/AHA screening

A

> 21 yo, every 5 years for low to moderate risk

More frequent for high risk

36
Q

ACC/AHA: Who to treat with statin?

A
  1. ASCVD
  2. LDL>190
  3. Diabetes: age 40-75, LDL >70
  4. 10 year risk >7.5%, age 40-75
37
Q

High intensity treatment medication.

A
  1. Atorvastatin 40/80
  2. Rosuvastatin 20/40

(Decrease LDL 50%)

38
Q

Who to treat high intensity?

A
  1. ASCVD up to age 75
  2. LDL > 190
  3. Diabetes, age 40-75, LDL >70, >7.5% risk
39
Q

Moderate intensity treatment medication.

A
  1. Atorvastatin 10-20
  2. Simvastatin 20-40
  3. Pravastatin 40

(Decrease LDL 30-50%)

40
Q

Who to treat moderate intensity?

A
  1. Age over 75

2. 40-75 yo, DM, LDL 70-189, 5-7.5% risk

41
Q

Statin MOA

A

Decrease rate limiting enzyme for cholesterol formation in cells.
HMG-CoA reductase inhibitor.

42
Q

Statin benefits/lipid effects

A 
Decrease all cause mortality
Decrease MI &amp; CVA
LDL 20-55%
TG 7-30%
HDL 5-15%
43
Q

Statin CI

A
  1. Pregnancy/Breastfeeding
  2. Liver disease/Unexplained LFT increase
    (Get baseline LFT)

Not effective: TG>400
Most effective: dose at night.

44
Q

Statin side effects

A
  1. Myalgias
  2. Rhabdomyolysis/Myopathy (check CK if at risk)
  3. Hepatotoxicity (Check baseline LFT)
  4. Increase risk for DM
45
Q

Cholesterol absorption inhibitor: MOA

A

Decrease absorption in intestine.

Increase LDL receptors peripherally.

46
Q

Cholesterol absorption inhibitor: Lipid effects

A

LDL 15-20%

47
Q

Cholesterol absorption inhibitor: CI

A
  1. With fibrates

2. Hepatic impairment

48
Q

Fibric acid derivates: MOA & names

A

Increase VLDL breakdown, decrease synthesis

Gemfibrozil, Fenofibrate

49
Q

Fibric acid derivates: Lipid effects

A

Drug of choice for TG>500
TG 40%
LDL 10-15%
HDL 15-20%

50
Q

Fibric acid derivates: Side effects

A
  1. Cholelithiasis
  2. Hepatits
  3. Myositis
51
Q

Fibric acid derivates: CI

A
  1. Gallbaldder ds
  2. Liver ds
  3. Caution-Pregnancy & Renal ds
  4. With Statin
52
Q

Niacin: MOA

A

Decrease VLDL production

53
Q

Niacin: Lipid effects

A

Good for very low HDL/mod high LDL
HDL 25-35%
LDL 15-25%
TG 50%

54
Q

Niacin: Side effects

A

Flushing

Long acting better tolerated

55
Q

Niacin: CI

A
  1. Pregnancy
  2. Liver ds
  3. Peptic ulcer
  4. Caution: Gout & DM
56
Q

Bile-acid binding resins: MOA/Names

A

Binds bile acids in intestine.
Decreases bile acids in entero-hepatic system.
Liver increases bile acid production.
Uses up cholesterol.

Names: Chole- Cole-

57
Q

Bile-acid binding resins: Lipid effects/who to us it in

A

LDL 15-25%
HDL insig
TG little/may increase

SAFE in pregnancy
Good for mod LDL & normal HDL/TG

58
Q

Bile-acid binding resins: side effects

A

GI upset/constipation

59
Q

Bile-acid binding resins: CI

A
  1. GI obstruction
  2. Hypertriglyceridemia
  3. Pancreatitis
60
Q

PCSK9 Inhibitor: MOA

A

Blocks LDL receptor degradation.

Is a monoclonal ab

61
Q

PCSK9 Inhibitor: Lipid effects, who to use

A

LDL 50-60%

Good for familial HLD

62
Q

Omega-3 fatty acids benefits

A

Improves TG, decreases CV, anti-inflammatory

63
Q

Familial hypercholesterolemia

A

LDL receptor dysfxn/gone

  1. Homo: LDL 8X, childhood
  2. Hetero: LDL 2X, 30s
64
Q

Familial hyperchylomicronemia

A

Abnormal lipoprotein lipase (enzyme allows tisue to take TG from VLDL/chylomicrons)
Severe TG

Foundations (7 decks)

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