Foundations II (Cholley) > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

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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
If TG greater than 200, what steps should be taken?
- Maximize statin therapy | - Consider Rx w/ non-statins
26
Screening according to ACC/AHA guidelines
- All adults ≥ 21 years - Repeat every 5 years for avg to low risk - Repeat more frequently if close to therapeutic thresholds
27
Tx recommendations according to ACC/AHA
Should undergo high intensity tx: - Anyone w/ ASCVD up to age 75 - Any adult w/ extremely elevated LDL (>190)
28
High intensity tx
Reduces LDL by 50% - Atorvastatin 40 or 80mg - Rosuvastatin 20 or 40mg
29
Tx recommendations for pts w/ DM?
- 40-75, LDL 70-189: Use moderate intensity | - < 40 or > 75 yo: Cost/benefit analysis
30
Moderate intensity tx
Reduces LDL 30% - Atorvastatin 10-20mg - Simvastatin 20-40mg - Pravastatin 40mg
31
Lifestyle changes: Diet
- AHA low fat diet - Mediterranean - Garlic, soy protein, vitamin C, pecans - Antioxidants * All combined - can lower LDL by 30%
32
Statins: MOA
Inhibit rate-limiting enzyme in formation of cholesterol
33
Statins: Fxn
Reduces fatal & non-fatal MI, incidence of CVA, & all-cause mortality*
34
HMG-CoA reductase inhibitors (aka - statins): Lipid effects
- *LDL decreases 20-55+% - HDL increase 5-15% - TG decrease 7-30%
35
HMG-CoA reductase inhibitors (statins): Contraindications
- Pregnancy/breastfeeding - Liver disease - Elevated LFTs - TG over 400-500mg
36
HMG-CoA reductase inhibitors (statins): Major side effects
- Myalgia - Myopathy, rhabdomyolysis - Hepatotoxicity - Increased diabetes risk
37
HMG-CoA reductase inhibitors (statins): Follow up
- LFTs | - Creatine kinase
38
Cholesterol absorption inhibitor: MOA
Decreases absorption of cholesterol in small intestine, upregulates LDL receptors on peripheral cells
39
Cholesterol absorption inhibitor: Lipid effects
LDL decreases 15-20%
40
Cholesterol absorption inhibitor: Contraindications
- Hepatic impairment - Do not use w/ fibrates - Ezetimibe
41
Fibric acid derivatives: MOA
Reduced synthesis & increased breakdown of VLDL particles
42
What is the drug of choice for those w/ TG > 500mg?
Fibric acid derivatives - Gemfibrozil - Fenofibrate
43
Fibric acid derivatives: Lipid effects
- LDL decrease 10-15% - HDL increase 15-20% - TG decrease 40%
44
Fibric acid derivatives: Side effects
- Cholelithiasis - Hepatitis - Myositis
45
Fibric acid derivatives: Contraindications
- Liver disease or permanent impairment - Gallbladder disease - Caution w/ pregnancy - Caution w/ renal impairment - Not recommended w/ statin use
46
Niacin
- Reduces production of VLDL particles - Short acting or long acting available - Ex. Niaspan, Slo-Niacin
47
Niacin: Lipid effects
- LDL decreases 15-25% - HDL increases 25-35% - TG decreases up to 50% - Best for moderately high LDL & very low HDL
48
Niacin: Contraindications
- Pregnancy/breastfeeding - Liver disease - Peptic ulcer - Caution w/ gout/ hyperuricemia - Caution w/ DM
49
Bile-acid binding resins: MOA
Reduction of bile acids in the entero-hepatic circulation causes liver to increase its production of bile acids, using hepatic cholesterol
50
Bile-acid binding resins: Lipid effects
- LDL decreased 15-25% - HDL – insignificant effect - TG – little effect or may increase
51
Bile-acid binding resins: Side effect
GI sx
52
Bile-acid binding resins: Contraindications
- Current or hx of GI obstruction - Hypertriglyceridemia - Pancreatitis
53
PCSK9 Inhibitors
- 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
Omega-3 fatty acids
- Improve TG, lower CV risk | - Anti-inflammatory
55
Familial hypercholesterolemia
- LDL receptors absent or dysfunctional - Homozygotes: LDL 8x normal - Heterozygotes: LDL 2x normal
56
Familial hyperchylomicronemia
Lipoprotein lipase abnormality - Enzyme that allows peripheral tissue to take up TG from chylomicrons & VLDL - Severe hypertriglyceridemia
57
Triglycerides: Transportation
- Transported through blood within lipoproteins | - Transported into skeletal muscle & adipose tissue to use as energy
58
Mild hypertriglyceridemia
200-499
59
Moderate hypertriglyceridemia
> 500
60
Severe hypertriglyceridemia
> 1000 | - Acute pancreatitis
Foundations II (Cholley)
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