Basic Principles Of Hemostasis Flashcards

1
Q

______ involves the enzymatic activation of series of plasma proteins (procoagulants) in the coagulation system to form fibrin meshwork

A

Secondary hemostasis

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2
Q

______ is a process whereby, on vessel injury, plasma proteins, tissue factors, and calcium interact on the surface of platelets to form a stable fibrin clot

A

Coagulation

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3
Q

Activated state of proenzymes is called?

A

Serine proteases

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4
Q

_____ occurs on the surface of platelet/endothelial cell membrane (platelet plug) & not on the fluid phase

A

Coagulation

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5
Q

_____ circulates in the plasma with vwf and is referred to as factor viii complex

A

Factor VIll

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6
Q

_____ is composed of large multimeric glycoprotein that participates in platelet adhesion and transports factor viii

A

Von willebrand factor

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7
Q

_____ are stored in the alpha granules in platelets and in weibel - palade bodies in ECs

A

Von willebrand factor (vwf)

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8
Q

Deficiency in factor viii or its dysfunction results in _____

A

Hemophilia A

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9
Q

Deficiency in VWF or a dysfunctional molecule results in?

A

Von willebrand disease (VWD)

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10
Q

_______ is a mineral & play a big role in the important stages of coagulation

A

Factor IV (calcium)

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11
Q

Enumerate the 3 acute phase reactants

A

Fibrinogen
HMWK
Prothrombin

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12
Q

_____ represents the antigenic properties of factor viii measured by immunoassays

A

Factor VWF:Ag-

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13
Q

_____ the property of VWF which causes platelet aggregation in the presence of ristocetin

A

Ristocetin co-factor activity

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14
Q

_______ consumed during coagulation, absent in serum but present in plasma. Vit. K not needed for their synthesis. Not absorbed by BaSO4 or Al(OH)3. Increased in inflammation, trauma, stress & pregnancy.

A

Thrombin-sensitive group/Fibrinogen group

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15
Q

______ is present in both serum and plasma (not consumed by coagulation), well-preserved in stored plasma. Vit. K needed for their synthesis, can be absorbed by BaSO4 & Al(OH)3.

A

Prothrombin group/Vit. K dependent group

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16
Q

_____ is a therapeutic inhibitor of Vit. K

A

Coumadin drugs

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17
Q

_____ is the basis for the oral anticoagulant ( warfarin, Coumadin) therapy

A

Vit. K antagonism

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18
Q

Enumerate the components of extrinsic tenase

A

VIIa
Tissue Factor
PPL
Ca

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19
Q

Enumerate the components needed for intrinsic tenase

A

IXa
VIIIa
PPL
Ca

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20
Q

Enumerate the components needed for prothrombinase

A

Xa
Va
PPL
Ca

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21
Q

____ is composed of factors XI, XII, prekallikrein, and HMWK.

A

Contact group

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22
Q

_____ is a non-enzymatic cofactor

A

HMWK

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23
Q

Enumerate the serine proteases

A

Kallikrein
IIa
VIIa
IXa
Xa
XIa
XIIa

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24
Q

Enumerate the cofactors/accelerators

A

Tissue factor
Va
VIIIa
HMWK

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25
Give the factor involved in substrate and transglutaminase/transamidase (note that both factors is different)
Substrate- factor I Transaglutaminase/transamidase - factor XIII
26
Enumerate the coagulation factors involved in contact group
XII XI Prekallikrein HMWK
27
Enumerate the coagulation factors involved in prothrombin group/Vit. K dependent group
II VII IX X
28
Enumerate the coagulation factors involved in fibrinogen group/thrombin sensitive group
I V VIII XIII
29
_____ bind, stabilize & enhance the activities of their respective enzymes
Cofactors/Accelerators
30
____ is the one that triggers tha extrinsic pathway
Thromboplastin
31
_____ is an activated coagulation factors which are the main players to produce fibrin clot
Serine proteases
32
Enumerate in order the 4 stages in coagulation
1.Contact phase 2. Activation of the common pathway 3. Conversion of prothrombin to thrombin 4. Formation of stable fibrin clot
33
______ is an assembly molecule needed in almost all phases of the intrinsic pathway
Phosphatidylserine
34
Why is it called INTRINSIC?
Because most factors involved here are found in the blood
35
This pathway starts with the activation of factor X to factor Xa by the intrinsic and extrinsic pathways.
Common pathway
36
Activation occurs when a vessel is injured, exposing the subendothelial tissues, basement membrane and collagen
Intrinsic pathway
37
Activated by the release of factor III into the plasma from injured tissues (collagen injury)
Extrinsic pathway
38
____ is a marker for thrombin generation
Prothrombin fragment 1.2
39
True or False: the 3 pathways do not fully describe how coagulation occurs physiologically
TRUE
40
Two phases of coagulation
Initiation Propagation
41
____ occurs in TF-expressing cells, produces 3-5% of the total thrombin generated
Initiation
42
_____-occuring in platelets, which produces 95% or more of the total thrombin
Propagation
43
Normal physiologic coagulation requires these 2 cell types:
1. Cell that express TF (extravascular) 2. Platelets (intravascular)
44
The 6N terminal assembles to form a bulky central region called
E domain
45
The 3 carboxyl terminals on each outer end of the molecule assembles to form two…
D domains
46
The cleaved fibrinogen is called
Fibrin monomer
47
In vivo, the endpoint of coagulation mechanism is ____
Stable fibrin clot
48
In vitro, the endpoint detected is ____
Fibrin polymer
49
_____ is the primary serine protease of the fibrinolytic system
Plasmin
50
______ is the main enzyme of the coagulation pathway
Thrombin
51
_____ is a protein produced by the liver and is a major inhibitor of blood coagulation.
Protein C
52
______ is a Vit. K dependent protein and also produced by the liver.
Protein S
53
______Inactivates the clotting cascade by inducing thrombin to activate PC
Thrombomodulin
54
T or F: When plasma C4bBP level increases, additional PS is bound and free PS levels become proportionally decreased, wc may increase the risk of thrombosis.
True
55
______ - major inhibitor of thrombin and Factor Xa. Its activity is enhanced by heparin to 2000x. The first inhibitor to be identified and the first to be assayed routinely
Antithrombin III/ antithrombin- a Serpin
56
Laboratory measurement of TAT is used as an indicator of _____
thrombin generation
57
_____ inhibits thrombin rapidly in the presence of dermatan sulfate, heparin sulfate, or heparin.
Heparin cofactor II (HC II)
58
____ inactivates Factor XIIa and kallikrein, Factor XIa and plasmin.
C1 inhibitor
59
________ - no clinical manifestation. It neutralizes the PPL reagent in APTT resulting to its prolonged result, which is why this is investigated by the physician.
Lupus anticoagulants
60
Enumerate the acquired hereditary inhibitors
Anti-VIII Anti-IX anti-X anti-V Anti-I anti-XIII anti-VWF
61
Enumerate the non- hereditary acquired inhibitors
Anti-VIII-postpartum, autoimmune disorder Acquired VWF disease Anti-IX Anti-XI Anti-V- related to Streptomycin therapy Anti-XIII- related to Isoniazid therapy Lupus anticoagulants