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30 Cards in this Set
- Front
- Back
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What tests can you use at the different stages of acute coronary syndromes?
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Asymptomatic (inflammation, plaque instability/disruption, reduced blood flow) = lipids, markers of inflammation coaguopathies, etc.
Unstable angina (myocardial ischemia) = cardiac proteins, natriuretic peptides, ischemia markers. Myocardial infarction (myocardial necrosis) = cardiac proteins, enzymes. |
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What are the different categories of lipoprotein classes?
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Chylomicrons (transport diet derived TG from gut,)
liver (liver derived TG transport,) IDL (LDL precursor,) LDL (cholesterol transport,) HDL (cholesterol removal.) |
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How is LDL's proatherogenic?
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LDL enters the cell and is modified, interacts with macrophages and various cytokines and causes plaques and fatty streaks.
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How is HDL atheroprotective?
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Prevents monocytes from adhering to the lumen, interacts with LDL and prevents it from becoming oxidized, removes cholesterol from the circulation.
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What are the routine lipid tests?
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Triglycerides, cholesterol, HDL-cholesterol, Non-HDL-C, and LDL cholesterol.
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Which tests are not yet routine but may be in the future?
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apoA-I and apoB, Lp(a), remnant lipoproteins, oxidized-LDL, oxidized-HDL, and lipoprotein subfractions.
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How good are lipid tests?
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Good! Very robust.
The most significant source of variation is biological. |
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How do you take a lipid testing sample?
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Fasting (10-12 h) sample required for full profile.
Serum or EDTA-plasma with no heparin! Heparin activates lipoprotein lipase and falsely lowers triglycerides. |
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What causes lipemia of the test tube?
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Triglycerides: chylomicrons and VLDL refract light. Not cholesterol!
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What lipids change drastically after a meal?
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Triglycerides change dramatically.
LDL-c and VLDL don't change very much. Cholesterol and HDL pretty much don't change at all. |
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What is the Friedewald equation?
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LDL = total cholesterol - (HDL + TGY/5)
Limitations: fasting, Tgy <400 |
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What are the advantages of direct assays?
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Good correlations, can usually measure when Tgy >400.
Heterogeneity influences accuracy, results vary between labs. |
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On what are the NCEP recommendations based?
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They are based on outcomes. They want to reduce illness/death from CHD.
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What is the relationship between LDL and CHD?
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For every 30 mg LDL, you have a 30% greater change of CHD.
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What are the primary and secondary therapeutic targets of cholesterol drug therapy?
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Primary therapeutic target: LDL cholesterol.
Secondary target: non-HDL cholesterol and apolipoprotein B. |
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What are the LDL targets?
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0-1 risk factor = <160,
2+ risk factors = <130, CHD = <100 |
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Should children be screened?
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If there is a family history of early CHD or one parent with cholesterol >240.
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What is ATP IV?
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ATP IV puts more focus on
Apo B (total) or Apo B-100, Non-HDL = total cholesterol - HDL |
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What do we know about LDL and HDL size and number?
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Smaller, denser LDL particles are more proatherogenic.
HDL2 is more atheroprotective than HDL3. NMR, ultracentrifugation, electrophoretic, and HPLC methods test this (not detected in routine tests.) For patients where there's a question about initiating drug therapy. |
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What bad forms of HDL are there?
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Discoidal HDL (LCAT deficiency)
Spherical HDL with impaired apo-A (myeloperoxidase, AGE in type I diabetes) |
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What primary lipid disorders are there?
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Defects in metabolic pathways: increased lipoprotein production, abnormal processing, defective cellular uptake)
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What secondary lipid disorders are there?
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More common.
Exogenous causes (drugs/alcohol,) endocrine/metabolic (diabetes, hypothyroid,) storage diseases (glycogen storage,) renal diseases (nephrotic syndrome,) liver diseases (congenital biliary atresia) |
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What are some things that trigger inflammatory response?
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Tobacco, HTN, hyperlipidemia, hyperglycemia.
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What is C-reactive protein?
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C-reactive protein is an activator of the classical complement pathway in response to stress, infection, trauma, neoplasm, etc.
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What are the proatherogenic characteristics of CRP?
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Monocyte/macrophage,
vascular smooth muscle cells, plaque, endothelial cells. |
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What is hsCRP?
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Not the same thing as CRP.
Divided into tertiles, high hsCRP + high troponin = VERY high morbidity. |
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What causes high hsCRP?
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Smoking, high BMI, insulin resistance.
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What are troponin and CK-MB levels used for?
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The level is related to risk of adverse event (MI/death) within 6-9 months.
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What patients often have cTn levels?
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Patients with renal disease.
More patients with chronic kidney disease die of CVD before they develop end-stage renal disease. |
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What are the possible mechanisms of troponin elevation in renal insufficiency?
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Hemodialysis, lack of clearance, subclinical ischemia/infarction, uremia, etc.
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