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Cardiopulmonary pathology > Lipoprotein & Atherogenesis > Flashcards

Lipoprotein & Atherogenesis Flashcards

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?

A

serotonin

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?

A

ApoB100

24
Q

hemodynamic stress

A

the frictional force acting endothelial cells as result of blood flow

25
Q

What are the results of endothelial dysfunction?

A

inflammation cytokines

lipoprotein entry & modification

26
Q

how does the foam cell formation occur?

A

unregulated uptake of modified LDL

& leukocyte recruitment

27
Q

What are two products that both lipoprotein modification & inflammatory cytokines both produce?

A

chemokines & leukocytes adhesion molecules

28
Q

what happen to endothelial cells when they are inflammed?

A

antithrombotic molecules decrease

vasodilators decrease

permeability to large molecules increase

inflammatory cytokines increase

leukocytes molecules increase

29
Q

What happen when smooth muscular cells migrate & proliferate in subendothelial space?

A

fibrous plague formation

30
Q

What are two substances that signal leukocyte recruitment?

A

chemokines

leukocyte adhesion molecules

31
Q

What happens to smooth muscular cells when they are inflammed?

A

inflammatory cytokines increase

migration and proliferation in the endothelial lining

extracellular synthesis increases

32
Q

The protein that is in all lipoproteins except LDL

What does it do?

A

ApoE

help inhibiting atherosclerosis development

33
Q

Events in atherogenesis

A

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
Q

What does oxidize LDL?

A

phagocytes secreted by macrophages & ROS (reactive oxygen species)

35
Q

When LDL is oxidized, what will it turn into?

A

foam cell

36
Q

After monocytes differentiate into macrophages, what do they secrete?

A

phagocytes that oxidized LDL

inflammatory cytokines

37
Q

What is the key step in atherogenesis event?

A

when LDL is oxidized to become foam cell

38
Q

How does LPL particle enter the sub-endothelial space?

A

Protein ApoB100 binds to negative charge of proteoglycans in matrix

39
Q

Where does unstable plague will rupture?

A

along the border with normal tissue where the hemodynamic stress is greatest

40
Q

What signals the VSMC to migrate and proliferate into sub-endothelial space?

A

inflammatory cytokines

41
Q

What does the VSMC do to streghthen the fibrous plague?

A

excrete more matrix proteins

42
Q

When does the fibrous plague begin?

A

when VSMC begin migrate and proliferate in sub-endothelial space

Cardiopulmonary pathology (12 decks)

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