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What is hyperlipidemia

elevation of total cholesterol AND triglycerides, the two main types of lipids


What do cholesterol and triglycerides do

Chol: helps form steroid hormones and bile acids
Tg: transfer energy from food to skeletal muscle/adipose


What are lipoproteins

how lipids are transported. That contain apoproteins and can be:
Low density (more TG)
High density (more APOPROTEIN)
-VLDL, IDL, LDL, HDL, and chylomicrons


What is the process of lipid transport (VLDL/LDL)

Liver uses TG and CHO to make VLDL
VLDL transfers TG to cells. less TG= becomes LDL
LDL provides Chol to cells
Excess LDL taken up by liver, cholesterol excreted into bile


Where is HDL made

liver and intestine
helps apoprotein transport by taking CHOL from the cells and bring to liver or other lipoproteins


What preventions exist for CVD

Primary: preventing HLD without risk for disease/diet
Secondary: preventing progression and managing disease


What is primary dyslipidemia

Genetic abnormality of cholesterol metabolism


What is secondary dyslipidemia

Dz develops secondary to:
DM, excess alcohol, hypothyroid, cholestatic liver dz, renal dz, smoking, obesity
Meds (OCP, thiazide, BB, atypical antipsychotics, protease inhibitors (HIV))


What do most clinics measure

Total Chol (LDL, VLDL, HDL)
----More difficult to measure VLDL and LDL so measure based on the above measurements


How can you tell what VLDL contains when calculating a lipid fraction

VLDL have 5x more Tg than chol
VLDL cholesterol= TG/5


How can you calculate LDL cholesterol

Total cholesterol- HDL cholesterol- TG/5


What are stipulations to calculating lipid levels

Pt must be fasting to give lowest TG
Tg level should be <400-500 (best LDL est. if TG <200)


What is ASVCD

When fatty materials collect in arterial walls and hardens over time
LDL can no longer put cholesterol into cells so it starts accumulating into plaques


What disorders can lead to ASCVD

Abnormal cholesterol metabolism disorders (genetic, insulin resistance, organ dysfunction)
Lifestyle factors (sat and trans-fat, obesity, smoking, high BP)


How does plaque formation occur

small dense LDL enters and sticks to artery wall, triggering cascade
LDL is oxidized, attracting macrophages
Endothelial dysfunction
--Usually not symptomatic (angina) until obstructive to blood flow


What can plaque rupture lead to

they are free to travel and can lodge in:
coronary arteries (MI)
brain (CVA/TIA)


What are the CVD risk factors

Non-modifiable (age, sex, race, FHx, etc.)
Modifiable (smoking, weight, diet, HTN, renal dz, low HDL)


What CVD risk factor calculators exist

Framingham risk score (what is the chance they will have a cardiac incident in the next 10 years) **Non-DM**
ACC/AHA risk score (what is the chance they will develop HD or stroke in the next 10 years)


What can lowering cholesterol reduce

Morbidity and mortality in men and women, middle aged and older


How does LDL reduction affect risk

1% LDL reduction= 1-1.5% CV risk reduction
2-3% HDL increase= 2-4% CV risk reduction


What evidence of CVD or secondary causes of HLD could you see on PE

elevated BP, BMI, waist circumference
Xanthomas, rashes
Corneal arcus, lipemia retinalis, AV nicking
Adventitious sounds in lungs
PMI, extra heart sounds
hepatomegaly, kidney mass, bruits
edema, PAD, diabetic foot
abnormal DTR


How do most HLD patients present

However, can have xanthomatous tendons, corneal arcus, lipemia retinals, xanthelasma, eruptive xanthomas


What are the NCEPP ATP III guidelines for treating ASCVD

1. Obtain fasting lipid profile (9-12 hours) LDL, HDL, total chol
2. ID CHD risk equivalents (CAD, PAD, AAA, DM)
3. Presence of major risk factors (smoking, HTN, HDL <40, FHx premature HD, men >45, women >55)
4. Use framingham for 10 year risk (>20% if w/ CHD risk equivalent) (10-20% if 2+RF) (<10% if 0-1 RF)
5. Determine risk category (CHD risk equivalent, LDL <70) (2+ RF, LDL <100) (0-1 RF, LDL <160)
6. Initiate TLC if LDL above goal (can reduce LDL 25-30%)
7. Add drug therapy if LDL still above goal after 3 mo.
8. ID (3+ RF) and treat metabolic syndrome
9. Treat elevated Tg and low HDL


What is the ATP III classification for lipids

LDL: optimal <100 (If with CAD, <70)
Total chol: desirable <200
HDL: low <40 (low women <50)

(step 9 says normal Tg are <150)


What factors make up TLC

AHA low fat diet (<30% kcal from fat, sat fat <7%)
Diet chol. intake <200 mg
Increase soluble fiber (10-25 g)
Add plant stanols
Aggressive weight management
Increase phys activity (30 min most days)


What are Metabolic Syndrome RF

Abdominal obesity (men >40, women >35)
TG >150
Low HDL (men <40, women <50)
High BP (>130/85)
Impaired fasting glucose (>100mg)


How can you treat elevated TG and low HDL (step 9)

TG: add nicotinic acid/fibrate to lower VLDL
If >200, statin therapy the add non-statins
HDL: exercise, increase MONOUNSATURATED fats, smoking cessation, mod EtOH intake (1-2xday)


What are the ACC/AHA guidelines on screening

Adults 21+
Every 5 years for low risk
More often if close to therapeutic threshold


Who does the ACC/AHA say SHOULD be treated with statins

Anyone with ASCVD
Adults with LDL >190 (extreme)
40-75 y/o w/ DM or LDL 70-189
40-79 y/o w/ 10 year risk >7.5%


What are the ACC/AHA HIGH intensity treatment recommendations

anyone with ASCVD
Adults w/ LDL >190
** treat w/ Atorvastatin (40/80) or Rosuvastatin (20/40)
Should reduce LDL 50% in 3 mo.