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Hemostasis I Flashcards

1
Q

What are the active pro-coagulant enzymes?

A

Serine proteases

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2
Q

What are the following co-factors that favor coagulation, i.e. the accelerants

  1. ) Soluble
  2. ) Cell-bound
A
  1. ) V and VIII

2. ) Tissue factor

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3
Q

Another accelerant co-factor is

A

Von Willebrand Factor

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4
Q

What are three anti-coagulant factors?

A

Thrombomodulin, Protein C, and Protein S

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5
Q

What is step one of hemostasis?

A

Local Vasoconstriction

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6
Q

The local vasoconstriction is caused by the release of the powerful vasoconstrictor

A

Endothelin

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7
Q

Step 2 of primary hemostasis is formation of the

A

Platelet plug

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8
Q

Hemostasis depends on

A

Platelet function

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9
Q

Platelets originate from the

A

Hematopoetic stem cells

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10
Q

Thrombopoiesis is regulated by the

A

Megakaryocyte

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11
Q

The platelet massis regulated by

A

Thrombopoietin

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12
Q

We see decreased platelet and megakaryocyte mass with increased

A

TPO

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13
Q

DNA replicates without nuclear or cell division

A

Endomitosis

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14
Q

A megakaryocyte nucleus MUST be polypoid to produce

A

Platelets

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15
Q

Platelets are formed in the bone marrow from

A

Megakaryocytes

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16
Q

What is a normal platelet count

A

150K to 350K

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17
Q

Characterized by too few platelets

A

Thrombocytopenia

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18
Q

Characterized by too many platelets

A

Thrombocytosis

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19
Q

Platelet size correlates with reactivity i.e. larger platelets are typically younger and are

A

Prothrombotic

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20
Q

Normal endothelial monolayer is

A

Anti-thrombogenic

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21
Q

Important for platelet adhesion when the endothelial monolayer is injured

A

von Willebrand Factor

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22
Q

A large circulating multimer, synthesized in endothelial cells and megakaryocytes

A

von Willebrand Factor

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23
Q

von Willebrand factor is stored in

A

Weibel-Pallade bodies

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24
Q

Plays an important role in both primary and secondary hemostasis

A

von Willebrand Factor (vWF)

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25
At the side of injury, vWF adheres to exposed
Collagen
26
Facilitates platelet tethering to subendothelial BM
vWF
27
With injury, vWF adheres to the vessel
Subendothelial matrix
28
With shear, vWF multimers uncoil, causing the adherence and activation of
Platelets
29
Activated platelets expose phosphatodyl serine and bind -to facilitate clotting
FVIII
30
Bleeding ceases by platelet-fibrin plug, sealing vascular injury and is followed by
Thrombolysis and tissue repair
31
Deficiency of GpIIb-IIIa complex causes
Glanzmann thrombasthenia
32
Deficiency of GpIb causes
Bernard-Soulier syndrome
33
Deficiency of vWF causes
von Willebrand disease
34
Activatedby adhesion and soluble mediators
Platelets
35
Resting platelets are smooth and disc shaped, while activated platelets have an
Irregular shape
36
Platelet aggregation occurs through binding of two
GPIIb/IIIa's
37
Primary hemostasis can be summarized as
Adhesion, Activation, and Aggregation
38
Adhesion is primarily through
vWF
39
Activation occurs primarily through
Collagen and ADP
40
Aggregation occurs primarily through
Fibrinogen, GPIIb/IIIa, and aIIbb3
41
What are three drugs that target platelet function improve outcome in patients with unstable angina
Aspirin, Thienopyridines, Glycoprotein IIb/IIIainhibitors
42
Blocks TXA2 production
Aspirin
43
Block ADP receptors (P2Y12)
Thienopyridines
44
Block platelet adhesion to fibrinogen/fibrin and vWF
Glycoprotein IIb/IIIainhibitors
45
Not normally active in circulation
Platelets
46
LOW platelet counts (<10 to 20K) result in
Petechiae
47
Reddish purple discolorations on the skin that do not blanche on applying pressure
Petechiae
48
Release trophic factors which maintain cell-cell contacts
Platelets
49
The initial platelet plug is not very
Strong
50
Thus, the platelet plug requires a strong
Sealant
51
An essential component of hemostasis is the formation of
Cross-linked fibrin
52
The process by which cross-linked fibrin is formed
Secondary hemostasis
53
The clotting cascade results in the formation of fibrinfrom
Fibrinogen
54
What are the three major classes of pro-coagultion players?
Serine proteases, cell-associated cofactors, and soluble cofactors
55
Serine proteases circulate as
Zymogens
56
An example of a cell-associated cofactor is
Tissue factor
57
Which three pro-coagulation players are NOT made in the liver?
Tissue factor, VIII, and vWF
58
Most coagulation factors are serine proteases that circulate as
Zymogens
59
When activated, coagulation factors are written with an
"a" i.e. X --> Xa
60
What are the two components of the Extrinsic hemostasis pathway?
Factor VII and tissue factor
61
What are the three components of the Intrinsic hemostasis pathway?
Factors IX, XI, and XII
62
What are the two components of the common hemostasis pathway?
Factor X and Factor II (prothrombin)
63
In the extrinsic pathway, vessel wall injury increases
Tissue factor expression
64
A transmembrane protein that is not normally accessible
Tissue Factor
65
Synthesized and expressed by endothelial cell AND monocytes
Transmembrane protein
66
Step 2 of the extrinsic pathway is tissue factor is bound by
Factor VII
67
Circulating Factor VII binds Tissue Factor (TF) and is activated, thus it becomes
Factor VIIa
68
Tissue Factor activates
Factor VII
69
Then Factor IX (9) is recruited to the complex and
Activated
70
Then, TF:FVIIa:FIXacomplex activates
Factor X
71
Then, FXaactivates Prothrombin (FII/2) to
Thrombin
72
Thrombin then cleaves fibrinogen to form
Fibrin
73
Step 4 is called
Amplification #1
74
During amplification #1, thrombin activated more
Factor IX and VIII
75
Anti-hemophilic factor activated by thrombin
Factor VIII
76
Factor VIII circulated in the plasma in a complex with
vWF
77
Links platelets to subendothelial BM
vWF
78
Binds to and stabilizes Factor VIII, extending half-life from 8 minutes to 8 hours
vWF
79
The most common inherited bleeding disorder
von Willebrand disease
80
Characterized by easy bruising, skin bleeding, and prolonged bleeding from mucosal surfaces
Von Willebrand Disease
81
A soluble co-factor with no enzymatic activity
Factor VIII
82
Factor VIIIa functions as an accelerant/catalyst for
Factor IXa
83
What is the clinical significance of the Factor VIII/IX complex?
Hemophilia A (VII) and Hemophilia B (IX)
84
Another soluble co-factor with no enzymatic activity that functions as an accelerant/catalyst for Factor Xa
Factor V
85
Factor IXa-VIIIacomplex generates LARGE amounts of activated
Factor X
86
Converts prothrombinto thrombin 300,000X faster than FREE factor Xa
Factor Xa-Va complex
87
What are the three pro-coagulant complexes that are essential to coagulation?
1. ) Tissue Factor::Factor VIIa::IXa≈ Factor X 2. ) Factor IXa::VIIIa≈ Factor X 3. ) Factor Xa::Va ≈ Factor II (Prothrombin)
88
Which pro-coagulant factors are dependent on Vitamin K?
Prothrombin (II) and Factors VII, IX,
89
Which anticoagulants are dependent on Vitamin K?
Proteins, C, S, and Z
90
Dependent on Vitamin K
Serine proteases
91
Vitamin K dependent factors have glutamate rich
N-terminus
92
Carboxylation of the GLU residues is required for
Activation
93
Carboxylation is dependent on
Vitamin K
94
The basis for anticoagulant action of sodium citrate
Blocking Ca2+
95
VitK2 is synthesized by colonic flora which can be disturbed by antibiotics leading to relative
Vitamin K deficiency
96
What are the two important forms of Vitamin K
Phylloquinone(K1) and Menaquinones(K2)
97
A drug that targets Vitamin K,was initially developed as a rodenticide
Warfarin
98
Action of warfarin is to block VitK dependent
Reductases
99
How is the intrinsic pathway activated?
Contact activation
100
Contact activation is independent of
Tissue Factor

Immunity (33 decks)

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