CPR 18 - Lipoproteins 2 Flashcards
Describe the basic structure and function of a HDL.
What apolipoprotein is required to form HDLs? Where does HDL synthesis take place?
What are HDLs major functions?
List the steps to reverse cholesterol transport.
Where is SR-B1 found besides the liver? Why?
It also found in tissues that synthesize steroid hormones because cholesterol is needed for steroid synthesis
How are cholesterol esters formed in the blood? What is required to activate this process?
What is CETP? What does it do and how?
How can CE (cholesterol esters) exchanged from HDL still reach the liver?
A VLDL will eventually become an IDL or LDL that will then be taken up by the liver.
What does a deficiency of CETP lead to?
High HDL-C (HDL cholesterol) and Low LDL-C (LDL cholesterol)
What is a hypolipidemia?
A low level of a specific lipoprotein
What is Hypoalphalipoproteinemia characterized by? What hereditary disease is it associated with? How can it be acquired?
What is Abetalipoproteinemia? What causes it? What are the clinical features of it?
It is a rare hereditary disease caused by an abnormal MTP (microsomal TAG transfer protein) which strongly reduces the release of VLDL and chylomicrons. Clinical features include a failure to thrive, fat malabsorption, steatorrhea, TAG accumulation in liver and intestine epithelia, acanthocytosis (RBC with spicules), retinitis pigmentosa, progressive blindness, and peripheral neuropathy due to Vitamin A & E deficiency.
What is hypobetalipoproteinemia?
A disease caused by apo B deficiency causeing no or very low LDL. Very similar outcomes as abetalipoproteinemia
What are the relevant blood tests and results for diagnosing Tangier disease?
HDL < 5mg/dL
What is the cause of Tangier disease? Explain how this causes all of the symptoms.
A genetic defect of the cholesterol (C) transporter ABCA1 which is responsible for pumping C out of cells and into the blood. This leads to very low free C levels which leads to HDL and apo A-1 degradation when they’re not sufficiently filled with CEs. This causes very low HDL levels. This also causes an accumulation of CEs in tissues and macrophage, seen as orange tonsils, enlarged liver and spleen, and corneal opacities. Peripheral neuropathy and permature MI are also commonly seen (30%).
What are the relevant blood tests and results for diagnosing Abetalipoproteinemia?
What is the normal fasting plasma TAG level? Which lipoprotein will be holding most of these TAGs?
What is the “total cholesterol” blood test looking for? What is the normal range?
What is a hyperlipidemia and what are the two we need to know?
What is a dyslipidemia and what blood test values indicate one?
What blood tests are done in a lipid profile screening for CVD risk factors?
How can LDL-C be calculated?
What are the primary causes of dyslipidemia?
What are the secondary causes of dyslipidemia?
How are the hyperlipidemias classified? Which classifications are most prevalent?
What are some clinical feature of Type 1: Familial Hyperchylomicronemia?
Facts to know about Type IIa: Familial Hypercholesterolemia
Facts to know about Type IIb: Familial Combined Hyperlipidemia
Facts to know about Type III: Dysbetalipoproteinemia
Facts to know about Type IV: Familial Hyperprebetalipoproteinemia.
Facts to know about Type V: Familial Mixed Hypertriacylglyerolemia
How can electrophoresis be used to identify hyperlipidemias?
What is the general goal when treating hypercholesterolemia? How can this be done?
What is the general goal when treating hypertriacylglyerolemia? How can this be done?
Describe the different types of LDL and which one is more detrimental and why.
What could LDL-pattern B result from?
Facts to know about Lp(a).
Summarize the risk factors for coronary heart disease.
