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Foundations II (Cholley) > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

What are the 2 main types of lipids? What do they do?

A
  1. Cholesterol: forms steroid hormones & bile acids

2. Triglycerides: transfer energy from food to cells

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2
Q

What is the fxn of lipoproteins?

A

Transport lipid

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3
Q

How are lipoproteins classified?

A

By density

  • Low = more triglycerides
  • High = more apoproteins
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4
Q

What are the 5 groups of lipoproteins?

A
  1. Chylomicron
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
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5
Q

Where is HDL made?

A

Liver & intestine

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6
Q

What is the fxn of LDL?

A

Provides cholesterol to cells

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7
Q

What happens as VLDL loses TG to cells?

A

LDL is created

*Excess is taken up by liver, cholesterol excreted into bile

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8
Q

Primary dyslipidemia

A

Genetic abnormality of cholesterol metabolism

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9
Q

What is associated w/ secondary dyslipidemia?

A
  • DM
  • Excessive alcohol use
  • Hypothyroidism
  • Cholestatic liver disease
  • Renal disease
  • Smoking
  • Obesity
  • Medications: OCPS, thiazide diuretics, beta blockers, atypical antipsychotics, protease inhibitors
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10
Q

What makes up total cholesterol?

A

HDL + VLDL + LDL

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11
Q

How do you calculate VLDL cholesterol?

A

Triglycerides ÷ 5

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12
Q

What is cardiovascular disease?

A

Fatty material collects in arterial walls, hardening over time

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13
Q

What causes ASCVD?

A
  • Excess cholesterol
  • Lifestyle factors:
    ˚Obesity
    ˚Smoking
    ˚BP
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14
Q

Plaque formation

A

LDL enters & sticks to artery wall

  • Triggers cascade of events:
    1. Oxidation of LDL
    2. Attracts macrophages (Foam cells)
    3. Endothelial dysfunction
    4. Vasoconstriction
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15
Q

What could plaque rupture lead to?

A
  • MI

- TIA or CVA

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16
Q

Hyperlipidemia signs & sx

A
  • Xanthomatous tendons
  • Corneal arcus
  • Lipemia retinalis
  • Xanthelasma
  • Eruptive xanthomas
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17
Q

What are non-modifiable risk factors for CVD?

A
  • Age: Men > 45, Women > 55
  • Sex
  • Family hx: premature heart disease in 1st degree relative (Men < 55, Women < 65)
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18
Q

What are modifiable risk factors of CVD?

A
  • HTN
  • DM
  • Dislipidemia
  • Kidney disease
  • Obesity
  • Smoking
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19
Q

What is optimal LDL according to ATP guidelines?

A

< 70 for those w/ CAD

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20
Q

What are major risk factors according to ATP?

A
  • Smoking
  • HTN
  • HDL < 40
  • Family hx of premature disease
  • Men > 45yo, Women > 55yo
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21
Q

What is optimal LDL for those w/ more than 2 risk factors, according to ATP?

A

< 100

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22
Q

If LDL is above goal, what are some lifestyle changes that can be suggested?

A
  • AHA low fat diet, < 30% total calories
  • Cholesterol intake < 200
  • Increased fiber (2g/day)
  • Plant stanols/ sterols
  • Weight management
  • Increased physical activity
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23
Q

Metabolic syndrome risk factors

A
  • Abdominal obesity
  • Triglycerides > 150
  • Low HDL
  • Increased BP
  • Impaired fasting glucose > 100
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24
Q

Tx for those w/ low HDL

A
  • Exercise
  • Increase monounsaturated fats*
  • Smoking cessation
  • Moderate EtOH use
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25
Q

If TG greater than 200, what steps should be taken?

A
  • Maximize statin therapy

- Consider Rx w/ non-statins

26
Q

Screening according to ACC/AHA guidelines

A
  • All adults ≥ 21 years
  • Repeat every 5 years for avg to low risk
  • Repeat more frequently if close to therapeutic thresholds
27
Q

Tx recommendations according to ACC/AHA

A

Should undergo high intensity tx:

  • Anyone w/ ASCVD up to age 75
  • Any adult w/ extremely elevated LDL (>190)
28
Q

High intensity tx

A

Reduces LDL by 50%

  • Atorvastatin 40 or 80mg
  • Rosuvastatin 20 or 40mg
29
Q

Tx recommendations for pts w/ DM?

A
  • 40-75, LDL 70-189: Use moderate intensity

- < 40 or > 75 yo: Cost/benefit analysis

30
Q

Moderate intensity tx

A

Reduces LDL 30%

  • Atorvastatin 10-20mg
  • Simvastatin 20-40mg
  • Pravastatin 40mg
31
Q

Lifestyle changes: Diet

A
  • AHA low fat diet
  • Mediterranean
  • Garlic, soy protein, vitamin C, pecans
  • Antioxidants
  • All combined - can lower LDL by 30%
32
Q

Statins: MOA

A

Inhibit rate-limiting enzyme in formation of cholesterol

33
Q

Statins: Fxn

A

Reduces fatal & non-fatal MI, incidence of CVA, & all-cause mortality*

34
Q

HMG-CoA reductase inhibitors (aka - statins): Lipid effects

A
  • *LDL decreases 20-55+%
  • HDL increase 5-15%
  • TG decrease 7-30%
35
Q

HMG-CoA reductase inhibitors (statins): Contraindications

A
  • Pregnancy/breastfeeding
  • Liver disease
  • Elevated LFTs
  • TG over 400-500mg
36
Q

HMG-CoA reductase inhibitors (statins): Major side effects

A
  • Myalgia
  • Myopathy, rhabdomyolysis
  • Hepatotoxicity
  • Increased diabetes risk
37
Q

HMG-CoA reductase inhibitors (statins): Follow up

A
  • LFTs

- Creatine kinase

38
Q

Cholesterol absorption inhibitor: MOA

A

Decreases absorption of cholesterol in small intestine, upregulates LDL receptors on peripheral cells

39
Q

Cholesterol absorption inhibitor: Lipid effects

A

LDL decreases 15-20%

40
Q

Cholesterol absorption inhibitor: Contraindications

A
  • Hepatic impairment
  • Do not use w/ fibrates
  • Ezetimibe
41
Q

Fibric acid derivatives: MOA

A

Reduced synthesis & increased breakdown of VLDL particles

42
Q

What is the drug of choice for those w/ TG > 500mg?

A

Fibric acid derivatives

  • Gemfibrozil
  • Fenofibrate
43
Q

Fibric acid derivatives: Lipid effects

A
  • LDL decrease 10-15%
  • HDL increase 15-20%
  • TG decrease 40%
44
Q

Fibric acid derivatives: Side effects

A
  • Cholelithiasis
  • Hepatitis
  • Myositis
45
Q

Fibric acid derivatives: Contraindications

A
  • Liver disease or permanent impairment
  • Gallbladder disease
  • Caution w/ pregnancy
  • Caution w/ renal impairment
  • Not recommended w/ statin use
46
Q

Niacin

A
  • Reduces production of VLDL particles
  • Short acting or long acting available
  • Ex. Niaspan, Slo-Niacin
47
Q

Niacin: Lipid effects

A
  • LDL decreases 15-25%
  • HDL increases 25-35%
  • TG decreases up to 50%
  • Best for moderately high LDL & very low HDL
48
Q

Niacin: Contraindications

A
  • Pregnancy/breastfeeding
  • Liver disease
  • Peptic ulcer
  • Caution w/ gout/ hyperuricemia
  • Caution w/ DM
49
Q

Bile-acid binding resins: MOA

A

Reduction of bile acids in the entero-hepatic circulation causes liver to increase its production of bile acids, using hepatic cholesterol

50
Q

Bile-acid binding resins: Lipid effects

A
  • LDL decreased 15-25%
  • HDL – insignificant effect
  • TG – little effect or may increase
51
Q

Bile-acid binding resins: Side effect

A

GI sx

52
Q

Bile-acid binding resins: Contraindications

A
  • Current or hx of GI obstruction
  • Hypertriglyceridemia
  • Pancreatitis
53
Q

PCSK9 Inhibitors

A
  • Monoclonal antibodies
  • Blocks PCSK9 effect of degrading LDL receptors
  • Lowers LDL by 50-60%
  • Administer by SC injection q 2-4 weeks
  • Alternative for non-tolerance of statins
54
Q

Omega-3 fatty acids

A
  • Improve TG, lower CV risk

- Anti-inflammatory

55
Q

Familial hypercholesterolemia

A
  • LDL receptors absent or dysfunctional
  • Homozygotes: LDL 8x normal
  • Heterozygotes: LDL 2x normal
56
Q

Familial hyperchylomicronemia

A

Lipoprotein lipase abnormality

  • Enzyme that allows peripheral tissue to take up TG from chylomicrons & VLDL
  • Severe hypertriglyceridemia
57
Q

Triglycerides: Transportation

A
  • Transported through blood within lipoproteins

- Transported into skeletal muscle & adipose tissue to use as energy

58
Q

Mild hypertriglyceridemia

A

200-499

59
Q

Moderate hypertriglyceridemia

A

> 500

60
Q

Severe hypertriglyceridemia

A

> 1000

- Acute pancreatitis

Foundations II (Cholley) (25 decks)

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