LEC3- PRIMARY HEMOSTASIS Flashcards

1
Q

what are the coag factors that are inactivated by the anti thrombin III

A

activated factor II, IX, X

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2
Q

factor X is also known as

A

Stuart- prower factor

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3
Q

it helps by activating protein C, while being binded to thrombin

A

thrombomodulin

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4
Q

the activated protein C will inhibits what factors

A

factor V and VIII (labile factors )

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5
Q

summarize how blood are being maintained not to clot unless there’s an injury

A

endothelial cells will produce PROSTACYCLIN and NITRIC OXIDE they both will inactivate the platelet to prevent it to adhere in endothelial cells

endothelial cell will release an another substance that is the Heparin sulfate. It will then bind to anti-thrombin III, anti-thrombin III will inhibit thrombin. Anti-thrombin III together with Heparin sulfate will inhibit or shutdown the activated Factor II, IX, and X

Lastly, it will produce thrombomodulin, will will bind to thrombin. Once protein C pass by, it will be enhanced and activated by thrombomodulin and will then bind with thrombin. They will then inhibit the labile factors which are the Factor V and VIII

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6
Q

it present a smooth contiguous surface

A

rhomboid cell of vascular epithelium

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7
Q

eicosanoid platelet inhibitor

A

prostacyclin

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8
Q

a vascular “relaxing” factor

A

nitric oxide

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9
Q

an anticoagulant that regulates thrombin generation

A

glycosaminoglycan heparin sulfate

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10
Q

a regulator of the extrinsic pathway of coagulation

A

TFPI - tissue factor pathway inhibitor

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11
Q

an integral component of the protein C control system

A

endothelial cell protein C receptor (EPCR)

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12
Q

a protein C coagulation control system activator

A

thrombomodulin

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13
Q

activated fibrinolysis

A

Tissue plasminogen activator (tPA)

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14
Q

what are the responses or mechanism that will occur once there’s a blood vessel damage

A

vascular response
platelet response
clotting system
fibrinolytic system

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15
Q

when there’s blood vessel damage, what are the responses under primary hemostasis>

A

vascular response - vasoconstriction
platelet response - adhesion and aggregation

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16
Q

is the primary response reversible?

A

yes, reversible and unstable

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17
Q

when there’s blood vessel damage, what are the responses under secondary hemostasis>

A

clotting system - through coagulation factors

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18
Q

when there’s blood vessel damage, what are the responses under tertiary hemostasis>

A

fibrinolytic system

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19
Q

are secondary hemostasis reversible?

A

nope, it’s irreversible and stable

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20
Q

what are needed to activate plasminogen to become plasmin and destroy the clot made during 2ndary hemostasis

A

fibrinolytic proteins

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21
Q

what are the platelet receptors needed

A

Gp Ib-IX-V

Gp IIb-IIIa

P2y12

TPa

Gp Ia
Gp VI

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22
Q

what is the receptor used for von willebrand factor?

A

Gp Ib-IX-V

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23
Q

receptor used for fibrinogen and vWF

A

Gp IIb-IIIa

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24
Q

receptor used for ADP

A

p2Y12

25
Q

receptor used for Thromboxane A2

A

Tissue plasminogen activator

26
Q

Receptor used for collagen

A

Gp Ia
Gp VI

27
Q

Basic Sequence of Events in Primary and
Secondary Hemostasis after Vessel Injury

A

vasoconstriction
platelet adhesion
platelet aggregation
fibrin-platelet plug formation
fibrin stabilization

28
Q

what factor can stabilize the fibrin clot?

A

factor XIII

29
Q

refers to the role of blood vessels and
platelets in the initial response to a
vascular injury or to the commonplace
desquamation of dying or damaged
endothelial cells

A

Primary Hemostasis

30
Q

they are the one responsible in primary hemostasis

A

blood vessels and
platelets

31
Q

Primary Hemostasis
Activated by desquamation and small injuries to blood vessels

true or false

A

true the fire

32
Q

Primary Hemostasis
➢Role of blood vessel and platelets in response to vascular injury

what is the products of primary hemostasis

A

➢Formation of platelet plug

33
Q

SUBSTANCESRELEASED in primarry hemostasis

A

Prostacyclin
Adenosine
Thrombomodulin
Heparin sulfate
tPA
Von Willebrand Factor
13-HODE ( 3-Hydroxyoctadecadienoic acid )

34
Q

13 HODE means

A

( 13-Hydroxyoctadecadienoic acid )

35
Q

how do vasoconstriction occurs during the vessel injury

A

endothelial cell will release a component called endothelin

this endothelin will bind to the smooth muscle receptor causing contraction and will cause vasoconstriction

36
Q

the binding of endothelin and smoothmuscle will inactivate ______ causing contraction

A

inactivates intracellular mechanism

37
Q

aside from the release of endothelin, we have another way of activating constriction, what are the 2nd and 3rd reason

A

myogenic reaction
pain receptor or noisy reaction

38
Q

what are the 3 causes of vasoconstriction

A

release of endothelin
myogenic reaction
nocireceptor/pain receptor

39
Q

this type of reaction leading to vasoconstriction in which there’s a direct damage or contact to the smooth muscle making it to contract

A

myogenic action

40
Q

this type of reaction leading to vasoconstriction in which where there’s inflammation, smooth muscle will release inflammatory chemicals leading to contraction

A

pain receptor

41
Q

o Converts plasminogen to qplasmin

A

tPA

42
Q

responsible in dissolution of clot

A

plasmin

43
Q

oEnhances activity of anti-thrombin III

A

*Heparan sulfate

44
Q

PARTS OF PLATELET PLUG FORMATION

A

*Primary hemostasis
* Secondary hemostasis
* Fibrinolytic system

45
Q

2 types of adhesion

A

direct
indirect

46
Q

a type of adhesion when there’s injury, the collagen explode
(there’s strong attraction between platelet and
collagen.

A

Direct

47
Q

the type of adhesion where the Von Willebrand factor will stick to the collagen when there’s injury and help
the platelet, to bind to it

A

Indirect

48
Q

platelets undergo shape changes with the intrusion of numerous pseudopods due to the _____

A

contraction of
microtubules.

49
Q

platelet release reaction is Stimulated by

A

o Collagen
o Thrombin
o Epinephrine
o Thromboxane A2

50
Q

Caused by the release of granules
and ADP from the adhering platelet

A

Initial Aggregation

51
Q

Platelets form a link or bridge Gp
IIb/IIa

A

secondary Aggregation

52
Q

Mediates ADP induced aggregation:

A

Gp IIb/IIIa with calcium and fibrinogen

53
Q

o Deficiency in aggregation results to what syndrome

A

Glanzmann’s
Thrombasthenia

54
Q

Thrombasthenia means

A

weak platelets

55
Q

vasoconstrictor and stimulates platelet
aggregation

A

Thromboxane

56
Q

Enables the vascular tissues or
vessels to close in order to conserve the
blood from getting out of the blood vessel.

A

Thromboxane A2

57
Q

Counterpart of prostacyclin

A

Thromboxane

58
Q
A