Nur 731 Hyperlipidemia

chol increases with age by 2 mg/dL per year during adulthood until age 65

before age 50, total chol higher for men with 2X CHD risk that women, until after menopause, then by age 60, same

only a small number of pts have monogenic abnormality but these acct for the most severe hyperlipidemias and the most aggressive CAD. Family screening should be done in these identified cases.

high in saturated fatty acids raises total and LDL, caloric excess and obesity affects triglycerides

thiazides increase LDL at least temporarily with doses over 50 mg/day.

cause slight HDL drop

causes increase in triglycerides.

can greatly increase serum lipids.

increases HDL. Inactivity and obesity drop HDL.

Smoking drops HDL

DM is assoc with high triglycerides and usually drops LDL

1 hypothyroidism,
2 nephritic syndrome
3 obstructive liver disease (increase total and LDL)

within 5 minutes of assuming a recumbent position, the TC levels drop to a max of 10-12% in 20-30 minutes.

Chronic stress or serious illness can cause a drop in the total, so better to measure after recovery from acute infections, tissue necrosis or surgery.

LDL + HDL + VLDL

total and HDL directly

by dividing TG concentration by 5 (as long as it’s under 400) and then derive LDL value.

all cholesterol subtypes: total cholesterol, total LDL, total HDL, and triglycerides as well as component HDL 2 and HDL 3, Lipo (a)
and LDL particle size

A

B which is more atherogenic), and gives estimation of patient’s possibility for metabolic syndrome.

q 5 years for adults >20 of total and HDL with additional test depending on screening results (i.e. complete lipid profile if TC > 240 or 200-240 with other CAD risk factors present) and if pts have evidence of CHD, do full profile

is an amino acid that influences blood clotting and alters endothelium

7.

Increasing folic acid and vitamin B sources in the diet (foods such as citrus fruits, grains, vegetables)

(Folgard, Foltx) which contain both Vit B6, B12 and folic acid (1-2.5 mg folic acid).

encourages cholesterol to build on vessel walls. Level is genetically induced.

high LDL levels

higher HDL levels, which also increase with regular cardio exercise.

smoking, obesity, hypertriglyceridemia. Single most powerful predictor of CHD risk and not too many therapeutic tools exist to increase HDL level.

hypothyroidism (check TSH), nephritic syndrome (urine protein), DM (glucose).

thiazides (increase LDL), beta blockers increase TG, postmenop ERT drops LDL and increases HDL and TG.

male over 45, woman over 55 or premature menopause not on HRT (which is most women), FH premature CHD (ie. MI or sudden death in first degree male relative <55 or woman < 65), current smoking, HTN, low HDL, DM.

dietary attention, reduce total fat, saturated fat, dietary chol (partially hydrogenated unsaturated FA)

serial measurement of serum lipids since biologic and analytic variations range 10-20%.

Use venous sample and send to lab with CDC standards.

LDL = total – [HDL + TG/5
, TG/5 + VLDL and usually 20% of TG level. Can’t measure LDL when TG exceeds 400 with standard profile, but not a problem with VAP testing.

lipids and protiens

the protien part of lpoprotiens

check total and HDL which can be nonfast without identified risk factors and with established risk factors, do a 12 hour fasting check of total, LDL, HDL and TG

is a marker of general inflammation

is more specific for endothelial inflammation.
How do you interpret hs CRP results?

first line is ASA, if not effective low or even higher dose (81 then 325) the statins lower it.

noncardiovascular problem and commence workup (CXR, abdominal sono, colonoscopy).

recommended.