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Terms in this set (18)
A The VLDL (very low-density lipoprotein) migrates in
the pre-β zone. The VLDL is about 50% triglyceride,
whereas LDL is only 10% triglyceride by weight. LDL
is formed from VLDL in the circulation. The process
is initiated by apoC-II on VLDL activating peripheral
lipoprotein lipase. Hydrolysis of triglycerides and
transfer of apoproteins from VLDL to HDL result in
formation of IDL. Larger IDLs are returned to the
liver as remnant lipoproteins. Further hydrolysis of
triglycerides, transfer cholesterol esters from HDL,
and transfer of apoproteins to HDL convert IDL
43. Following ultracentrifugation of plasma, which
fraction correlates with pre-β lipoprotein?
A. Very low-density lipoprotein (VLDL)
B. Low-density lipoprotein (LDL)
C. High-density lipoprotein (HDL)
A The VLDL is formed in the liver largely from
chylomicron remnants and hepatic-derived
triglycerides. Therefore, the VLDL transports the
majority of endogenous triglycerides, while the
triglycerides of chylomicrons are derived entirely
from dietary absorption.
Select the lipoprotein fraction that carries most of
the endogenous triglycerides.
C About 50% of the weight of HDL is protein, largely
apo A-I and apo A-II. The HDL is about 30%
phospholipid and 20% cholesterol by weight.
The HDL binds and esterifies free cholesterol from
cells and transports it to the liver, where it can be
eliminated in the bile.
The protein composition of HDL is what
percentage by weight?
A. Less than 2%
A Apoprotein A-I and apo A-II are the principal
apoproteins of HDL, and low apo A-I has a high
correlation with atherosclerosis. Conversely,
apo-B100 is the principal apoprotein of LDL, and an
elevated level is a major risk factor in developing
coronary heart disease. Apoprotein assays are not
recommended as screening tests because they are
not as well standardized as LDL cholesterol assays.
However, apo-B100 assay is more sensitive than LDL
cholesterol in predicting coronary artery disease
risk. Apo-B100 may be abnormal in persons with
increased small dense LDL. Small dense LDL is more
atherogenic than large LDL molecules. In addition,
persons with hyperapobetalipoproteinemia
overproduce apo-B100 without having significantly
elevated LDL cholesterol.
Which apoprotein is inversely related to risk of
coronary heart disease?
A. Apoprotein A-I
B. Apoprotein B100
C. Apoprotein C-II
D. Apoprotein E4
C IDLs have roughly equal amounts of cholesterol
and triglyceride. The IDL has a density of about
1.006-1.020, causing it to float on the 1.063 density
potassium bromide solution used to recover LDL
by ultracentrifugation. IDL has faster electrophoretic
mobility on agarose than beta lipoprotein. These
observations gave rise to the terms "floating
beta" and "broad beta," respectively. Familial
dysbetalipoproteinemia is in part caused by a
polymorphism of apoE (apo-E2) that has poor
affinity for the apo-E receptor on hepatocytes.
Not all persons with the homozygous polymorphism
develop the disease; thus, other factors are
necessary for the accumulation of IDL.
In familial β dyslipoproteinemia (formerly
type III hyperlipoproteinemia), which lipoprotein
B The production of excess insulin leads to
hypertriglyceridemia and is one mechanism
responsible for familial endogenous
hypertriglyceridemia. ApoC-II is an activator of
lipoprotein lipase, and a homozygous deficiency
results in high plasma chylomicrons and VLDL.
ApoE3 deficiency is synonymous with inheritance of two apo-E2 alleles that lead to β dyslipoproteinemia.
Familial hypercholesterolemia is inherited as an
autosomal dominant trait. The classical form results
from one of many mutations affecting the LDL
receptor that cause it to have a lower affinity for LDL.
A related hypercholesterolemia common in people
of European ancestry results from a mutation of the
apo-B100 gene that causes LDL to have a lower
affinity for the LDL receptor. Together, they make
familial hypercholesterolemia the most common
inherited hyperlipoproteinemia with a frequency
Which of the following mechanisms accounts
for the elevated plasma level of β lipoproteins
seen in familial hypercholesterolemia (formerly
type II hyperlipoproteinemia)?
B. ApoB-100 receptor defect
C. ApoC-II activated lipase deficiency
D. ApoE3 deficiency
B Deficiency of capillary endothelial lipase is the
most common cause of fasting chylomicronemia.
This lipase is also known as post-heparinactivated
lipase and apo C-II-activated lipase.
β Glucocerebrosidase deficiency results in
accumulation of glucocerebrosides and is
the cause of Gaucher's disease. ApoC-II deficiency
results in decreased activity of peripheral
and hepatic lipases and is associated with
hypertriglyceridemia. Apo-B deficiency resulting
from a point mutation in the apo-B gene, is
responsible for hypobetalipoproteinemia, and is
inherited as an autosomal dominant trait. LDL
levels are about half normal in heterozygotes,
and this reduces their risk of coronary artery
Which enzyme deficiency is most commonly
associated with familial hypertriglyceridemia
associated with fasting plasma cholomicrons
(formerly type I hyperlipoproteinemia)?
A. β Glucocerebrosidase deficiency
B. Post-heparin-activated lipoprotein lipase
C. Apo-B deficiency
D. Apo-C-III deficiency
A The conditions listed are very commonly encountered
causes of secondary hyperlipoproteinemia. Oral
contraceptives, pregnancy, and estrogens may cause
secondary hypertriglyceridemia owing to increased
VLDL and endogenous triglycerides. Hypothyroidism
and obstructive hepatobiliary diseases are usually
associated with secondary hypercholesterolemia
owing to high LDL. Diabetes mellitus and chronic
pancreatitis may produce hypertriglyceridemia,
chylomicronemia, or mixed hyperlipidemia.
Which of the following conditions is most
consistently associated with secondary
C. Oral contraceptive therapy
D. Diabetes mellitus
D Deficiency of apo A-I is seen in Tangier disease, a
familial hypocholesterolemia. Heterozygotes have
about half of the normal level of HDL (familial
hypoalphalipoproteinemia) and homozygotes
have almost no detectable HDL. Tangier disease
is caused by a mutation of the ATP-binding
cassette gene. The deficient gene prevents apo A-I
from binding lipids, and it is rapidly catabolized.
Abetalipoproteinemia results from defective
hepatic transport of apo-B100, and is also inherited
as an autosomal recessive condition. LDL is absent,
and the condition is associated with hemolytic
anemia and central nervous system damage.
Which of the following is associated with Tangier
A. Apoprotein C-II deficiency
B. Homozygous apo-B100 deficiency
C. Apoprotein C-II activated lipase
D. Apoprotein A-I deficiency
D There are 7 subfractions of LDL and 10 subfractions
of HDL. These are grouped into subclasses defined
by their molecular sizes. In general, the small, dense
LDL subclasses contain more oxidized LDL and are
more atherogenic than the larger LDL molecules.
The larger HDL subfractions comprising the HDL-3
subclass are associated with a lower risk of coronary
Which of the following statements is correct?
A. Both HDL and LDL are homogenous
B. There are several subfractions of LDL but
C. There are several subfractions of HDL but
D. There are several subfractions of both HDL
C Because LDL cholesterol, HDL cholesterol, VLDL
cholesterol, and triglycerides are all risk factors for
coronary artery disease, NCEP recommends a fasting
lipid profile to include triglycerides, total cholesterol,
HDL cholesterol, and LDL cholesterol be performed
every 5 years beginning at age 20. However, because
LDL cholesterol is the target of treatment, therapeutic
goals are based on the LDL cholesterol. New
guidelines recommend an LDL cholesterol goal
below 70 mg/dL for the highest-risk persons.
What is the lipid testing protocol for adults
recommended by the National Cholesterol
Education Program (NCEP) to evaluate risk for
atherosclerosis beginning at age 20?
A. Total cholesterol, fasting or nonfasting every year
B. Total cholesterol, fasting, every 2 years
C. Lipid profile, fasting, every 5 years
D. LDL cholesterol, fasting, every 2 years
C Lipid orders that include triglyceride and LDL
cholesterol should always be performed using a
plasma or serum specimen collected after a
12-14 hour fast. The patient should be instructed
to drink nothing but water during this period.
Fasting specimens are preferred for total and
HDL cholesterol as well, but nonfasting specimens
may be used for initial screening purposes.
What is the most appropriate fasting procedure
when a lipid study of triglyceride, total cholesterol,
HDL cholesterol, and LDL cholesterol tests are
A. 8 hours; nothing but water allowed
B. 10 hours; water, smoking, coffee, tea (no sugar
or cream) allowed
C. 12 hours; nothing but water allowed
D. 16 hours; water, smoking, coffee, tea (no sugar
or cream) allowed
C NECP has identified LDL cholesterol as the target of
therapy for reducing the risk of heart attack because
lowering LDL cholesterol has proven to be an
effective intervention. The greater the risk of coronary
heart disease, the lower the cutpoint for intervention.
For persons at high risk (a 10-year risk of heart attack
> 20%) the cutpoint is ≥ 100 mg/dL for initiation of
statin therapy. For highest-risk persons (those that
have acute coronary syndrome, and multiple or
uncontrolled risk factors) the treatment goal is LDL
cholesterol below 70 mg/dL.
Treatment recommendations for patients with
coronary heart disease are based upon
measurement of which analyte?
A. HDL cholesterol
C. LDL cholesterol
D. Total cholesterol
B The HDL cholesterol cutpoint recommended by
NCEP is < 40 mg/dL regardless of sex. A result
below 40 mg/dL counts as a risk factor for coronary
artery disease. Conversely, if the HDL cholesterol
is ≥ 60 mg/dL, then one risk factor is subtracted
from the total number. The therapeutic goal for
someone with low HDL cholesterol is still reduction
of LDL cholesterol (if elevated), weight loss, and
What is the HDL cholesterol cutpoint recommend
A. <30 mg/dL
B. <40 mg/dL
C. <30 mg/dL for males and < 40 mg/dL
D. <45 mg/dL for males and < 50 mg/dL
C NCEP recommends a 12-hour fasting sample when
screening persons for risk of coronary artery disease.
However, if a fasting sample is unavailable, NCEP
recommends performing the total cholesterol
and HDL cholesterol because these tests are least
affected by recent ingestion of food. If the total
cholesterol is ≥ 200 mg/dL or the HDL cholesterol
is < 40 mg/dL, then testing for LDL cholesterol and
triglycerides should be performed when a fasting
sample can be obtained. An EDTA plasma sample
is acceptable for most enzymatic cholesterol and
An EDTA blood sample is collected from a
nonfasting person for a CBC. The physician
collected the sample from the femoral vein because
venipuncture from the arm was unsuccessful. He
called the lab 15 minutes after the sample arrived
and requested a lipid study including triglyceride,
total cholesterol, HDL cholesterol, and LDL
cholesterol. Which test results should be used to
evaluate the patient's risk for coronary artery
A. Total cholesterol and LDL cholesterol
B. LDL cholesterol and triglyceride
C. Total cholesterol and HDL cholesterol
D. Total cholesterol and triglyceride
C The diseases mentioned result from inborn errors of
lipid metabolism (lipidoses) caused by deficiency of an
enzyme needed for lipid degradation. Specific lipids
accumulate in the lysosomes. Niemann-Pick disease
results from a deficiency of sphingomyelinase;
Gaucher disease from β-glucocerebrosidase; Fabry
disease (sex linked) from α-galactosidase A; and
Tay-Sachs from N acetylglucosaminidase A.
Which of the following diseases is caused by a
deficiency of sphingomyelinase?
A. Gaucher disease
B. Fabry disease
C. Niemann-Pick disease
D. Tay-Sachs disease
B Enzymatic methods for triglyceride measurement
are widely used because they eliminate the need
for extraction and saponification. However, they are
subject to positive interference from endogenous
glycerol and variations in the efficiency of lipase,
which can result in under- or overestimation of
triglycerides. The most accurate method for
triglyceride assay is the nonenzymatic method
based upon reaction of formaldehyde with
chromotropic acid. In this method, extraction with
silicic acid and chloroform separates triglycerides
from lipoproteins, phospholipids, and glycerol.
Saponification with alcoholic potassium hydroxide
(KOH) produces glycerol, which is oxidized to
formaldehyde by periodate. The formaldehyde
reacts with chromotropic acid to form a pink
Which method is considered the candidate
reference method for triglyceride measurement?
A. Glycerol kinase-ultraviolet
B. CDC modification of van Handel and Zilversmit
C. Hantzsch condensation
D. Glycerol kinase coupled to peroxidase
C All enzymatic triglyceride methods require lipase to
hydrolyze triglycerides, and glycerol kinase to
phosphorylate glycerol, forming glycerol-3-phosphate.
The most common method couples glycerol kinase
with glycerol phosphate oxidase and peroxidase.
1. Triglyceride + H2O Lipase glycerol + fatty acids
2. Glycerol + ATP GK glycerol-3-phosphate + ADP
3. Glycerol-3-phosphate + O2
phosphate + H2O2
H2O2 + phenol + 4-aminophenazone Px
quinoneimine dye + H2O
GK = glycerol kinase; GPO = glycerol phosphate
oxidase; Px = peroxidase
Which of the following enzymes is common to all
enzymatic methods for triglyceride measurement?
A. Glycerol phosphate oxidase
B. Glycerol phosphate dehydrogenase
C. Glycerol kinase
D. Pyruvate kinase
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