Lipoprotein & Atherogenesis Flashcards

(42 cards)

1
Q

what are the components of lipoprotein?

what are the major lipoproteins?

A

phospholipid, cholesterol, apoprotein, tryglyceride & cholesteryl esters

HDL, LDL, IDL, VLDL & chylomicrons

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2
Q

What type of lipoprotein considered to be bad?

Why?

A

LDL

because it has the highest % cholesterol of its components

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3
Q

What major protein is LDL made of?

A

ApoB100

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4
Q

Protein ApoB48 are exclusively in what lipoprotein?

A

chylomicrons

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5
Q

What type of protein only found in HDL?

A

ApoD

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6
Q

ApoE

What type of lipoproteins is this protein in?

A

proteins that help inhibiting the developmen of atherosclerosis

all lipoproteins except LDL

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7
Q

What are the primary proteins in HDL?

A

ApoA I & II

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8
Q

What does ApoA I & II do?

A

activate LCAT, which convert free cholesterol into cholesteryl esters

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9
Q

What are the endothelium-derived vasodilator?

vasoconstrictor?

A

Ach, shear stress, serotonin & thrombin

thrombin, angiotensin II & epinephrine

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10
Q

thrombosis

what does it cause?

A

the development of blood clot inside the vessels

obstructing the blood flow

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11
Q

Mechanism against the thrombosis

A

inactivation of thrombin by antithrombin III

Inactivation of factor V & VIII by protein C+ S

______ VII & tissue complex

______ VIIa by TFPI & complex Xa

lysis of fibrin by plasminogen activator

Inactivation of platelets activation

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12
Q

what are substances that endothelial-derived vasodilator influence?

A

NO

prostacyclin

EDHF

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13
Q

How does prostacyclin inhibit the platelet activation?

A

increase lvl of cAMP

increase blood flow & minimize contact btw thrombogenic factors

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14
Q

How does cell uptake the cholesterol?

A

ApoB100 binds to LDL-R and undergo endocytosis

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15
Q

thrombus

A

the blood clot

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16
Q

What factors do protein C+S inhibit in mechanism against thrombosis?

A

Factor V + VIII

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17
Q

What hormone can act as vasodilator if there is damage to vessel?

18
Q

atherogenesis

A

the formation of abnormal fat deposits within the arterial walls of blood vessels

19
Q

What are the causes of atherogenesis?

A

the endothelial or vascular smooth muscular cells dysfunction

20
Q

What cause the endothelial dysfunction?

A

chemical irritants or hemodynamic stress

21
Q

What is the effect of increase lvl of cAMP to platelets?

A

inhibit platelet aggregations & adhesion

22
Q

What are two vasodilators that help against thrombosis?

A

NO

prostacyclin

23
Q

What from what protein that Apo48 is derived from?

24
Q

hemodynamic stress

A

the frictional force acting endothelial cells as result of blood flow

25
What are the results of endothelial dysfunction?
inflammation cytokines lipoprotein entry & modification
26
how does the foam cell formation occur?
unregulated uptake of modified LDL & leukocyte recruitment
27
What are two products that both lipoprotein modification & inflammatory cytokines both produce?
chemokines & leukocytes adhesion molecules
28
what happen to endothelial cells when they are inflammed?
antithrombotic molecules decrease vasodilators decrease permeability to large molecules increase inflammatory cytokines increase leukocytes molecules increase
29
What happen when smooth muscular cells migrate & proliferate in subendothelial space?
fibrous plague formation
30
What are two substances that signal leukocyte recruitment?
chemokines leukocyte adhesion molecules
31
What happens to smooth muscular cells when they are inflammed?
inflammatory cytokines increase migration and proliferation in the endothelial lining extracellular synthesis increases
32
The protein that is in all lipoproteins except LDL What does it do?
ApoE help inhibiting atherosclerosis development
33
Events in atherogenesis
1) LDL particles pass into sub-endothelial cells 2) LDL is oxidized by ROS and oxidizing enzymes secreted by macrophages 3) monocytes are attracted to site by chemo-attractant molecules 4) Monocytes differentiate into macrophages & secrete inflammatory cytokines 5) secreted inflammatory cytokines & PDGF activate smooth muscle cells to migrate & proliferate in sub-endothelial space
34
What does oxidize LDL?
phagocytes secreted by macrophages & ROS (reactive oxygen species)
35
When LDL is oxidized, what will it turn into?
foam cell
36
After monocytes differentiate into macrophages, what do they secrete?
phagocytes that oxidized LDL inflammatory cytokines
37
What is the key step in atherogenesis event?
when LDL is oxidized to become foam cell
38
How does LPL particle enter the sub-endothelial space?
Protein ApoB100 binds to negative charge of proteoglycans in matrix
39
Where does unstable plague will rupture?
along the border with normal tissue where the hemodynamic stress is greatest
40
What signals the VSMC to migrate and proliferate into sub-endothelial space?
inflammatory cytokines
41
What does the VSMC do to streghthen the fibrous plague?
excrete more matrix proteins
42
When does the fibrous plague begin?
when VSMC begin migrate and proliferate in sub-endothelial space