Hyperlipidemia Flashcards
What are the different types of lipids and what do they do?
Cholesterol: helps form steroid hormones & bile acids
Triglycerides: helps transfer energy from food to cells
How are lipids transported? How are they classified by density?
- Lipoproteins, which contain proteins called apoproteins
- Low density = more triglycerides
- High density = more apoproteins
What are the 5 major groups of Lipoproteins based on density from largest to smallest?
Bad or Non-HDL: Chylomicron and Chylomicron remnant, very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), low density lipoprotein (LDL)
Good: high density lipoprotein (HDL)
What is hyperlipidemia? List 2 other names for it.
HLD: elevation of both total cholesterol and triglycerides
-dyslipidemia & dyslipoproteinemia
Describe the transport of lipids.
- Liver uses fat and cholesterol stores to make VLDL.
- VLDL transfers TG to cells
- LDL is created as it looses TG
- LDL provides cholesterol to cells
- Excess LDL taken up by the liver, helps trigger formation of plaque
- HDL made in liver and intestine will work against process by removing excess cholesterol from blood and tissue cells
- HDL gives VLDL back some of this cholesterol, which turns it back to LDL
- liver removes LDL from bloodstream & converts its cholesterol to bile acid
What are 4 examples of cardiovascular diseases?
- Coronary heart dz (CHD)
- Peripheral artery dz. (PAD)
- Aortic atherosclerosis & thoracic or AAA
- Cerebrovascular dz
What is the difference between primary and secondary prevention of CVD?
primary: pt has no evidence of ASCVD
secondary: goal is the prevention of a 2nd event
What is the difference between primary and secondary dyslipidemia?
Primary: genetic abnormality of cholesterol metabolism
Secondary: DM, ETOH use, hypothyroidism, cholestatic liver dz, renal dz, smoking, obesity, medications (OCPs, thiazide diuretics, BetaBlockers, atypical antipsychotics, protease inhibitors)
How is cholesterol carried?
Total cholesterol = HDL + VLDL + LDL
Most clinical labs measure…? How do they calculate VLDL Cholesterol?
- total cholesterol, triglycerides, and HDL
- VLDL cholesterol = Triglycerides / 5
How do you ensure the pt gives the lowest TG level? Why is this important?
- MUST be fasting
- if TG is elevated over 200mg/dL the estimation of LDL will be way off
What is ASCVD? How is it started and how is it enhanced?
- when fatty material collects in arterial walls, hardening over time
- started by excess cholesterol (VLDL & LDL): genetic, insulin resistant, organ dysfunction
- enhanced by lifestyle: saturated fats/trans-fats, obesity, smoking, BP
Describe the process of plaque formation.
- small/dense LDL enters and sticks to artery wall
- triggers cascade of events: 1) oxidation of LDL -proinflammatory, thrombotic 2) attracts macrophages - foam cells
3) endothelial dysfunction 4) vasoconstriction
What happens if a plaque ruptures in the bloodstream?
- MI in coronaries
- TIA or CVA in the brain
Note: pt doesn’t feel pain until plaque ruptures so often goes undetected
Give examples of non-modifiable and modifiable cardiovascular risk factors
Non: age (M >45yo & F >55yo), sex, family hx of premature heart dz in 1st degree relative (M >55yo & F >65yo)
Mod: dyslipidemia, kidney dz, obesity, HDL, HTN, DM, diet, smoking
What percent of the pt population have CVD diagnoses and CVD deaths under the age of 65 y/o?
dx = 50% deaths = 15%
Compare and contrast Framingham and ACC/AHA CVD risk scores.
- Fram: 10yr risk for MI or death
- A/A: 10yr risk for heart dz or CVA, race (AA/other), DBP, DM
- Both: total & HDL cholesterol
What is the relationship between lipids & CVD risk?
- inc. LDL = inc ASCVD risk
- inc. HDL = dec ASCVD risk
- primary prevention –> moderate benefits
- secondary prevention –> strong data
- for each 1% reduction in LDL –> 1-1.5% reduction in risk of major cardiovasc. events. (even treating mild elevated LDL is beneficial)
- for each 2-3% increase in HDL –> 2-4% reduction in risk of major cardiovasc events
List some examples of secondary causes associated with lipid abnormality.
- obesity, sedentary lifestyle, DM, ETOH use, nephrotic syndrome, hypo/hyperthyroid, Cushing, diuretics, BBs meds
What are some characteristic PE findings for evidence of CVD or 2ndary causes of HLD
VS: waist circumference Skin: xanthomatous tendons, eruptive xanthomas HEENT: lipemia retinalis, corneal arcus Heart: PMI? extra sounds Abdomen: hepatomegaly, kidney masses Extremities: foot exam (DM), PAD?, edema
NCEPP ATP III guidelines
Steps:
1) determine lipoprotein levels after 9-12 hr fast
2) identify clinical atherosclerotic dz that results in H risk for CHD
3) determine risk factors other than LDL
4) if 2+ risk factors present w/out CHD or risk eq. –> asses 10yr w/ Framingham’s
5) Determine risk category
6) start TLC (therapeutic lifestyle changes) if LDL is above goal
7) consider adding drug therapy if it remains above goal
8) identify metabolic syndrome and treat if 3 mo of TLC not working
9) treat elevated triglycerides and low HDL
What is an optimal LDL level for a patient with CAD? optimal HDL?
- LDL = < 70mg/dL but otherwise 100
- HDL = <40 M or <50 F
What is step 2 in the ATP III guidelines for hyperlipidemia?
Identify presence of clinical atherosclerotic disease that confers high risk for CHD events (CHD risk equivalent) CAD PAD AAA DM
What are the major risk factors in Step 3 ATP III guidelines?
- smoking
- HTN
- HDL < 40mg/dL
- family hx of premature coronary dz
- men > 45 and women >55 yrs
What is the 4th step in the ATP III guidelines?
if 2+ factors present w/out CHD or risk eq., asses 10 yr CHD risk (Framingham)
- > 20% CHD risk eq.
- 10-20%
- <10%
What is the 5th step in the ATP III guidelines?
determine risk category.
- CHD or risk eq w/ 10yr >20%: treat LDL down to <100 or (<70 optional); >100 start TLC; if >130 then drug therapy
- 2+ risk factors w/ 10yr <20%: treat LDL down to <130; if >130 then TLC but if 10-20% CHD risk then drug; if less than 10% CHD risk then >160 drug therapy
- 0-1 Risk factor: <160 LDL goal; >160 TLC; >190 drug
