Block 3 Lipoproteins Sem 1
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Higher levels in the blood are correlated with a decreased risk of heart disease.
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VLDL
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Albumin
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Chylomicrons
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HDL
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IDL
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Explore the fundamentals of lipoproteins with a focus on LDL in 'Block 3 Lipoproteins Sem 1'. This quiz assesses knowledge on LDL's metabolic routes, its functions, and clinical implications in conditions like familial hypercholesterolemia, enhancing understanding for students and professionals.
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- 2.
Which statement below best describes the metabolic route of LDL ?
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VLDL are acted on by lipoprotein lipase to form HDL which is converted to LDL.
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VLDL are acted on by lipoprotein lipase to form IDL which is converted to LDL
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It is made in the liver from chylomicron remnants
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It is made in plasma from HDL.
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Chylomicrons are acted on by lipoprotein lipase to form remnants which are converted to IDL and then LDL in plasma.
Correct Answer
A. VLDL are acted on by lipoprotein lipase to form IDL which is converted to LDLExplanation
LDLs result from the maturation of VLDLs to IDLs and finally to LDLsRate this question:
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- 3.
What is the defect seen in patients with familial hypercholesterolemia (FHC)?
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The LDL contains too much cholesterol to bind to the receptor.
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The LDL contains a defective apo B100.
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The lysosomes contain no cholesteryl esterase
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The patient has no activator for the lipoprotein lipase
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The patient has a defective receptor
Correct Answer
A. The patient has a defective receptorExplanation
A genetic defect; lack of functional receptor precludes proper processing, and LDL levels increase to pathologic levelsRate this question:
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- 4.
Activator of LCAT:
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Apo C-II.
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Apo B100.
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Apo A-I.
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Apo E
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All of these.
Correct Answer
A. Apo A-I.Explanation
Apo A-I is a key co-factor for LCAT.Rate this question:
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- 5.
What is the rationale for trying to lower LDL by use of cholestyramine?
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It is a competitive inhibitor of lipoprotein lipase
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It decreases the number of class B type I Scavenger Receptors in fibroblasts
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It down-regulates the synthesis of LDL receptors in liver.
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It stimulates ACAT in cells and so depletes cellular free cholesterol.
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It stimulates bile acid excretion in the feces.
Correct Answer
A. It stimulates bile acid excretion in the feces.Explanation
Elimination of bile from the GI tract means that the liver must make more bile salts and will therefore need more cholesterol precursor, which can be recovered from the blood by increasing the number of liver LDL receptors.Rate this question:
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- 6.
Which statement below about LDL is FALSE?
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High levels indicate an increased risk of coronary artery disease
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Its receptor binds to both apoB-100 and apoE
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Its major apo protein is apoE.
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On electrophoresis it migrates faster than chylomicrons.
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The use of resins will upregulate LDL receptors on the surface of liver cells
Correct Answer
A. Its major apo protein is apoE.Explanation
Apo B100 is the major apoprotein found in LDLsRate this question:
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- 7.
Which statement below about lipoprotein lipase is FALSE ?
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It is absent in blood vessels found in adipose tissue.
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It is attached to a glycosaminoglycan
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It is responsible for hydrolysis of triglycerides
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VLDL is one of its substrates
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It requires apoprotein CII be present for activity
Correct Answer
A. It is absent in blood vessels found in adipose tissue.Explanation
Lipoprotein lipase is attached to the capillary endothelium in adipose tissue, lactating breast tissue and skeletal muscle tissue.Rate this question:
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- 8.
Which statement below concerning LDL and oxidized LDL is TRUE?
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Endothelial cells reduce oxidized LDL to native LDL.
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Foam cells are formed during endothelial cell processing of LDL.
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Oxidized LDL is chemotactic for monocytes
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Free radicals containing oxygen prevent buildup of atherosclerotic plaques by destroying LDL.
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NONE of the above is TRUE.
Correct Answer
A. Oxidized LDL is chemotactic for monocytesExplanation
Excess LDL passes through the endothelial barrier and may be oxidized leading to a chemotactic attraction of monocytes (macrophages). The oxidized LDL undergoes phagocytosis by the macrophages thereby yielding a foam cell. Ultimately these cells undergo cell death and lysis leading to injury to the endothelial cells, with resultant metabolic processes that lead to atherosclerosisRate this question:
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- 9.
Why is the rate of production of LDL increased in familial hypercholesterolemic (FHC) individuals?
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Because IDL is removed more slowly from the circulation and so is converted into LDL.
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Because VLDL synthesis is increased
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Because IDL synthesis is increased
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Because chylomicron synthesis is increased.
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ALL of the above are correct
Correct Answer
A. Because IDL is removed more slowly from the circulation and so is converted into LDL.Explanation
Decreased lipoprotein receptors or receptor occupancy leaves the IDLs in the blood stream where they are converted to LDLs. Remember that IDLs bind to those receptors that recognize ApoE including the LDL receptor. FHC individuals lack working LDL receptors.Rate this question:
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- 10.
Binds to a specfic cell receptor and is found on IDL but not on LDL.
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Apo C-II
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Apo B100
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Apo B48
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Apo E.
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Apo A-I
Correct Answer
A. Apo E.Explanation
Apo B and Apo E are found on IDL but Apo E is not on LDL.Rate this question:
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- 11.
Which ONE of the following proteins allows HDL to off-load cholesterol esters?
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Lipoprotein Lipase.
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LCAT
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ACAT
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ApoAI
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Scavenger Receptor Class B Type I.
Correct Answer
A. ApoAIExplanation
An apoA-I mimetic peptide facilitates off-loading cholesterol from HDL to liver cells through scavenger receptor BI.
Excessive cellular cholesterol is transported to the liver by a pathway called 'reverse cholesterol transport.' Scavenger receptor class B, type I (SR-BI) mediates cholesterol uptake in the liver
LCAT functions in the plasma and forms CE in HDL by transferring polyunsaturated fatty acid from phosphatidylcholine to cholesterol.Rate this question:
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Current Version
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Mar 16, 2023Quiz Edited by
ProProfs Editorial Team -
Nov 07, 2011Quiz Created by
Chachelly
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