Hyperlipidemia Flashcards
1
Q
What are the 2 main types of lipids? What do they do?
A
- Cholesterol: forms steroid hormones & bile acids
2. Triglycerides: transfer energy from food to cells
2
Q
What is the fxn of lipoproteins?
A
Transport lipid
3
Q
How are lipoproteins classified?
A
By density
- Low = more triglycerides
- High = more apoproteins
4
Q
What are the 5 groups of lipoproteins?
A
- Chylomicron
- VLDL
- IDL
- LDL
- HDL
5
Q
Where is HDL made?
A
Liver & intestine
6
Q
What is the fxn of LDL?
A
Provides cholesterol to cells
7
Q
What happens as VLDL loses TG to cells?
A
LDL is created
*Excess is taken up by liver, cholesterol excreted into bile
8
Q
Primary dyslipidemia
A
Genetic abnormality of cholesterol metabolism
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
10
Q
What makes up total cholesterol?
A
HDL + VLDL + LDL
11
Q
How do you calculate VLDL cholesterol?
A
Triglycerides ÷ 5
12
Q
What is cardiovascular disease?
A
Fatty material collects in arterial walls, hardening over time
13
Q
What causes ASCVD?
A
- Excess cholesterol
- Lifestyle factors:
˚Obesity
˚Smoking
˚BP
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
15
Q
What could plaque rupture lead to?
A
- MI
- TIA or CVA
16
Q
Hyperlipidemia signs & sx
A
- Xanthomatous tendons
- Corneal arcus
- Lipemia retinalis
- Xanthelasma
- Eruptive xanthomas
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)
18
Q
What are modifiable risk factors of CVD?
A
- HTN
- DM
- Dislipidemia
- Kidney disease
- Obesity
- Smoking
19
Q
What is optimal LDL according to ATP guidelines?
A
< 70 for those w/ CAD
20
Q
What are major risk factors according to ATP?
A
- Smoking
- HTN
- HDL < 40
- Family hx of premature disease
- Men > 45yo, Women > 55yo
21
Q
What is optimal LDL for those w/ more than 2 risk factors, according to ATP?
A
< 100
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
23
Q
Metabolic syndrome risk factors
A
- Abdominal obesity
- Triglycerides > 150
- Low HDL
- Increased BP
- Impaired fasting glucose > 100
24
Q
Tx for those w/ low HDL
A
- Exercise
- Increase monounsaturated fats*
- Smoking cessation
- Moderate EtOH use
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
