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Flipped Classroom: Lipoproteins I Flashcards

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1
Q

Lipoproteins are rich in

A

Cholesterol and triglycerides

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2
Q

Can vary over a greater range than glucose

A

Lipid levels

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3
Q

Hypercholesterolemia is usually a result of

A

High LDL/HDL ratios

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4
Q

Leads to narrowing of artery walls, decreased blood and oxygen supply to the heart, and possibly heart attack and death

A

Hypercholesterolemia

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5
Q

In population studies, there is a very strong correlation between plasma LDL cholesterol and the incidence of

A

Coronary Artery Disease (CAD)

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6
Q

What percentage of adult Americans have atherosclerotic narrowing of their coronary arteries?

A

70%

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7
Q

Contain cholesterol-laden foam cells, and their location depends on the cause of the dyslipidemia

A

Xanthomas

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8
Q

Patients with hypercholesterolemia but no hypertrygliceridemia have

A

Tendon xanthomas (achilles and hands/fingers)

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9
Q

Patients with combined hypercholesterolemia and hypertriglyceridemia have

-form over joints

A

Tuberous xanthomas

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10
Q

Yellowish cholesterol deposits under the skin of the eyelids are known as

A

Xanthelasmas

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11
Q

Xanthelasmas are most commonly seen in patients with high

A

LDL cholesterol

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12
Q

The type of LDL that leads to plaque formation

A

Oxidized LDL

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13
Q

The initiation of an atherosclerotic plaque involves which three stages of development?

A
  1. ) Fatty streak formation
  2. ) Conversion to fibrous plaque
  3. ) Alteration to complex lesion
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14
Q

Lined by a monolayer of endothelial cells that is in contact with blood overlying a basement membrane

A

Tunica intima

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15
Q

The initial steps of atherosclerosis includes the recruitment of monocyte-macrophages to the subendothelial space and the infiltration of

A

Oxidized plasma LDLs

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16
Q

These oxidized LDLs are taken up by macrophages, leading to the formation of

A

Foam cells

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17
Q

A these cholesterol laden foam cells accumulate, we see further recruitment of

A

Monocyte-macrophages

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18
Q

Release cytokines an growth factors that lead to smooth muscle cell proliferation and synthesis of extracellular matrix molecules such as collagen, elastin, and proteoglycan

A

Monocyte-macrophages

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19
Q

These changes form the earliest lesion of atherosclerosis, known as the

A

Fatty streak

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20
Q

Fatty streaks form in most people by the age of 20 in the

A

Aorta and coronary arteries

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21
Q

Plaque macrophages and smooth muscle cells can die in advancing lesions by

A

Necrosis and apoptosis

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22
Q

A mixture of lipid and subintimal smooth muscle that grows into the lumen

A

Atheroma

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23
Q

In a complicated lesion, the endothelial cell layer covering the lesion is lost. As a result, the surface of the lesion becomes

A

Thrombogenic (induces clot formation)

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24
Q

This results in an increase in cellular debris and the appearance of calcification and

A

Cholesterol crystals

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25
Lastly, the complicated lesion emerges with calcification and further damage to the arterial wall and alterations in the structure of the
Fibrous cap
26
This leads to complete occlusion of the artery, called
Infarction
27
Also we can see disruption of the plaque and thrombosis, leading to
Stroke
28
A metabolic disorder caused by a mutation in the DHCR7 gene on chromosome 11
Smith-Lemli-Opitz Syndrome (SLOS)
29
This DHCR7 gene codes for an enzyme that is involved in the production of
Choleterol
30
Are unable to make enough cholesterol to support normal growth and development
SLOS patients
31
Shows the facial features of microcephaly, ptosis, broad nasal ridge, upturned nose, and micrognathia (small jaw)
SLOS
32
The most frequently reported clinical finding in the limbs of SLOS patients is
Syndactyly of the 2nd and 3rd toes
33
Cleft palate, short thumbs, and polydactyly are also signs of
SLOS
34
In a steady state individual, the normal levels of cholesterol can be twice the normal levels of
Glucose
35
Consists of four fused hydrocarbon rings (A-D) called the "steroid nucleus"
Cholesterol
36
Cholesterol has an 8 carbon branched hydrocarbon chain attached to
Carbon 17 of the D ring
37
Ring A of cholesterol has a hydroxyl group at
Carbon 3
38
Ring B of cholesterol has a double bond between carbons
5 and 6
39
Most plasma cholesterol is in an esterified form. I.e it has a
Fatty acid attached to carbon 3
40
A very hydrophobic compound
Cholesterol
41
Not found in membranes, and are normally only present in small amounts in most cells
Esterified cholesterol
42
Because of their hydrophobicity, cholesterol and its esters must be transported in association with a protein component (lipoprotein) or be solubilized by
Phospholipids and bile salts
43
The body's supply of cholesterol, derived from the diet and de novo synthesis is always transported in the blood packaged into
Lipoprotein particles
44
The lipoprotein particle derived form the intestine is the
Chylomicron
45
The lipoprotein particle derived from the liver is the
VLDL
46
Part of the exogenous pathway of lipoprotein metabolism
Chylomicron
47
Part of the endogenous pathway of lipoprotein metabolism -seen before in the context of de novo synthesized TAGs
VLDLs
48
Takes place in the cytosol of virtually all cell types
Cholesterol synthesis
49
The two major organs that contribute de novo cholesterol to the body's pool
Liver and intestine
50
The source for all carbon atoms in cholesterol
Acetyl-CoA
51
The major co-factor required for cholesterol synthesis is
NADPH
52
Also consumed during cholesterol synthesis
ATP
53
The rate limiting step in cholesterol synthesis is catalyzed by
HMG CoA reductase (HMGR)
54
The rate limiting step of cholesterol synthesis, catalyzed by HMG CoA reductase produces
Mevalonic acid (releases free CoA)
55
The rate limiting step of cholesterol synthesis, catalyzed by HMG CoA reductase uses up
2 NADPH
56
The formation of mevalonic acid is the step of cholesterol synthesis that is
Regulated
57
Mevalonic acid gives rise to isoprene squaline, which 'folds up' and through a series of intramolecular reactions gives rise to
Lanosterol
58
Mevalonic acid gives rise not only to cholesterol, but also to
Terpenes (isoprenoids/isoprenes)
59
Farnesyl pyrophosphate, dolichol, ubiquinones, and geranyl pyrophosphate are the terpenes we get from
Mevalonic acid
60
Can be conjugated with proteins and then serve as lipid anchors
Farnesyl pyrophasphate and geranyl pyrophosphate
61
Can be reduced to ubiquinols which can donate their electrons to the electron transport chain
Ubiquionones
62
Excess cholesterol activates -makes cholesterol esters
ACAT
63
Stimulates the proteolysis of HMG CoA reductase and influences RNA polymerase II's rate of HMG-CoA reductase mRNA synthesis
Cholesterol
64
Stimulates the activity of HMG-CoA reductase
Insulin
65
Inhibits the activity of HMG-CoA reductase
Glucagon and cholesterol
66
Inhibits the uptake of cholesterol into liver cells
Excess cholesterol
67
Reduces the levels of HMG-CoA reductase through stimulation of its degredation
Cholesterol
68
Makes the cholesterol ore hydrophobic, enabling it to be packaged and stored and transported more easily
Esterification
69
In epithelial cells of the intestine, some cholesterol is converted to cholesterol ester by
ACAT
70
Hepatocytes and steroid producing cells store cholesterol as cholesterol esters inside lipid droplets in the
Cytosol
71
Uses a fatty acid from the phospholipid lecithin (phosphatidylcholine) on a peripheral cell to esterify cholesterol to cholesterol esters
Lecithin cholesterol acyltransferase (LCAT)
72
In the blood, LCAT is bound to
HDL
73
Regulation of HMGR through covalent modification occurs as a result of
Phosphorylation and dephosphorylation
74
HMGR is most active in the
Unphosphorylated form
75
Phorphorylated by AMP-activated protein kinase (AMPK) which decreases its activity
HMGR
76
Negatively affect cholesterol biosynthesis by increasing the activity of the inhibitor of phosphoprotein phasphatase inhibitor-1 (PPI-1)
Glucagon and epinephrine
77
Stimulates the removal of phasphates and thereby activates HMGR
Insulin
78
Cholesterol synthesis is trancriptionally controlled by
SREBP2
79
A cholesterol sensor that is the main regulator of HMGR activity
Sterol Regulatory Element Binding Protein (SREBP2)
80
An integral membrane protein of the ER that senses the concentration of cholesterol in the ER membrane
SREBP2
81
When the concentration of cholesterol in the ER is abnormally low, SREBP-containing visicles form and move to the
Golgi apparatus
82
There, proteases cleave
SREBP2
83
The N-terminal segment of SREBP2 then moves into the nucleus and enhances transcription of several genes, including the genes for
HMGR and also LDL receptors
84
When cholesterol levels are high, there is no stimulation of
SREBP2
85
HMGR is the target of a very widely used class of drugs called
Statins
86
Structural homologues of HMGR and compete for HMG-CoA binding on the reductase, reducing its ability to promote cholesterol synthesis
Statins
87
An exampleof a statin is
Lovastatin
88
Lower blood cholesterol levels while also restoring the liver cholesterol pool
Statins
89
The liver accomplishes this by upregulating the quantity of
LDL receptor molecules on hepatocytes
90
In a small subset of the population, statins can result in profound
Myopathy
91
Prescribed both as a preventative and in respone to CAD and MI
Statins
92
Most lipids are transported in the blood as part of soluble complexes called
Lipoproteins (LPs)
93
Plasma LPs are spherical particles composed of a hydrophobic lipid core surrounded by a
Hydrophilic layer
94
The lipid core contains primarily
Triglycerides (TG) and Cholesterol Esters (CE)
95
Composed of amphipathic lipids such as phospholipids, unesterified cholesterol, and special proteins called apolipoproteins or apoproteins
External layer of lipoproteins
96
These proteins facilitate lipid solubilization and help to maintain the structural integrity of
LPs
97
Serve as ligands for LP receptors and regulate the activity of LP metabolic enzymes
Apolipoproteins and apoproteins
98
What are the 4 major categories of lipoproteins?
1. ) Lipoproteins 2. ) VLDL 3. ) LDL 4. ) HDL
99
The largest lipoproteins but the least dense due to the large amount of triacylglycerides in these molecules
Chylomicrons
100
The smallest lipoproteins but the most dense due to low lipid and high apoprotein content
HDL

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