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What is dyslipidemia?
Any abnormal concentration of lipid (C, CE, or TAG) in the blood
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What is hyperlipidemia?
- elevated levels of lipids in the blood
- =hyperlipoproteinemia
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What is hypolipidemia?
- reduced levels of lipids in the blood
- =hypolipoproteinemia
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What is primary dyslipidemia?
dyslipidemia caused by an inherent defect in lipoprotein metabolism
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What is secondary dyslipidemia?
dyslipidemia caused by another disease (ex. obesity, diabetes mellitus, hypothyroidism)
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What is the most common serum profile of dyslipidemia?
hypertriacylglycerolemia and reduced levels of HDL cholesterol
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Why is a blood sample taken after a 12 hour fast?
to make sure there are no CM from the previous meal
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What is the Friedwald Equation?
LDL-C = Total-C - VLDL-TAG/5 - HDL-C
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What is type IIa hyperlipidemia?
Cause?
Lipid panel?
Prevalence
Symptoms?
Treatment?
- Elevated LDL, familial hypercholesteremia
- Deficiency of LDL receptor expression
- Increase of LDL, elevated C, normal TAG
- Heterozygous common, homozygous rare
- Xanthomata (accumulation of lipids) on extremities, corneal arcus, atherosclerosis; risk of cardiovascular disease
- Diet; reduce intake of cholesterol and fat, combination therapy (HMG-CoA reductase inhibitor = statin and absorption inhibitor, also in combination with niacin
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What is type I hyperlipidemia?
Cause?
Lipid panel?
Prevalence?
Symptoms?
Therapy?
- Familial chylomicronemia (elevated CM)
- Deficiency in lipoprotein lipase and/or Apo C-II synthesis or function
- Elevated fasting CM, TAG elevated (fasting plasma turbid with milky CM forming creamy top layer, C normal
- Rare
- Eruptive xanthomata, hepatosplenomegaly, pancreatitis
- No drug therapy, only dietary fat restriction, fat soluble vitamin supplements, diet with medium and short chain TAG (tropical oils) avoid CM production
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What is type IV hyperlipidemia?
Cause? Primary? Secondary?
Lipid panel?
Prevalence?
Symptoms?
Treatment?
- Elevated VLDL, familial hypertriglyceridemia
- Primary-VLDL overproduction and/or decreased VLDL removal, Secondary-obesity, ethanol intake, estrogen use, insulin resistance
- Common (1 in 300)
- Serum opaque, few clinical manifestations, if C elevated=elevated risk of cardio-vascular disease
- Correct secondary causes by diet/life style changes, combination therapy
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What is type IIb hyperlipidemia?
Causes? Primary? Secondary?
Lipid Panel?
Prevalence?
Symptoms?
Treatment?
- Elevated LDL and VLDL, familial combined hyperlipidemia
- Primary-overproduction of Apo B-100, Secondary-cluster of precipitating factors; obesity, glucose intolerance, insulin resistance, hypertension
- Elevated VLDL, TAG elevated, LDL elevated, C elevated, HDL usually decreased
- Common (1 in 200)
- No xanthomata, high risk of premature CVD
- Aggressive treatment, diet, life style, weight loss, combination therapy
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What is type III hyperlipidemia?
Cause?
Lipid panel?
Prevalence?
Symptoms?
Treatment?
- Elevated IDL, familial dysbetalipoproteinemia
- Polymorphism of Apo E gene(ligand for hepatic Apo E receptor)
- VLDL remnants (=IDL) and CM remnants elevated, TAG and C elevated
- Rare
- Tuberoeruptive and/or striate palmar xanthomata, premature coronary and peripheral vascular diseases
- Diet, combination therapy
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What are scavenger receptors (type A)?
Receptors on macrophages for damaged LDL (insensitive to cholesterol levels=continuos uptake of damaged LDL
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What do macrophages (foam cells) release that leads to an atherosclerosic plaque?
Cytokines (stimulate inflammation, immune response, collagen synthesis, proliferation of smooth muscle cells, accumulation of calcium)
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What are the two best treatments for reducing LDL-C?
Statins (HMG CoA reductase inhibitors) and Resins
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What are two of the best ways to increase HDL-C levels?
- Fibrates (increase expression of Apo A-I)
- Niacin (decrease catabolism of Apo A-I)
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What is abetalipoproteinemia (CM retention disease)?
- Loss of function, mutation in gene encoding MTP (microsomal transfer protein)
- MTP: transfers lipids to nascent CM and VLDL before they are released from enterocytes and hepatocytes
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What is Tangier disease (alphalipoprotein deficiency)?
Defect in ATP binding cassette protein A1 (ABC-A1)
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What does ATP binding cassette protein A1 (ABC-A1) do?
Transfers C from peripheral cells to HDL
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