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Finals > Hema-Lec-Hemostasis > Flashcards

Hema-Lec-Hemostasis Flashcards

1
Q

Complex physiologic process

A

Hemostasis

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2
Q

Simple physiologic process of hemostasis

A

Injury—>produces a clot to stop the bleeding—> Confines the clot to the site of injury—>Finally dissolves the clot as the wound heals

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3
Q

absence of a single
plasma procoagulant

A

Anatomic hemorrhage

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4
Q

Absence of a control protein leads to (5)

A

thrombosis,
stroke, pulmonary embolism, deep vein thrombosis and cardiovascular events

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5
Q

Continues bleeding

A

Hemorrhage

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6
Q

Too much clotting

A

Thrombosis

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7
Q

Major systems of hemostasis

A

Blood vessels
Platelets
Plasma protein

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8
Q

Major systems of hemostasis purpose

A

To prevent, predict, diagnose and manage hemostatic disease

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9
Q

For clot formation

A

Platelets

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10
Q

Helps to avoid excess clot formation

A

Plasma protein

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11
Q

Hemostasis interaction of

A

 Vasoconstriction
 Platelet adhesion and aggregation
 Coagulation enzyme activation

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12
Q

Interaction of
 Vasoconstriction
 Platelet adhesion and aggregation
 Coagulation enzyme activation
Purpose

A

=To stop bleeding

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13
Q

Vasoconstriction is triggered by?

A

Serotonin

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14
Q

Key cellular elements

A

 Cells of the vascular intima
 Extravascular tissue factor (TF) – bearing cells
 Platelets
 ***plasma components are the coagulation and
fibrinolytic proteins and their inhibitors

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15
Q

***plasma components are the?

A

coagulation and
fibrinolytic proteins and their inhibitors

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16
Q

Blood vessels and platelets response

A

Primary hemostasis

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17
Q

involves the interaction of vasoconstriction, plate- let adhesion and aggregation, and coagulation enzyme activa- tion to stop bleeding

A

Hemostasis

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18
Q

The key cellular elements of hemostasis are the?

A

cells of the vascular intima
extravascular tissue factor (TF)–bearing cells
platelets

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19
Q

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

A

Primary hemostasis

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20
Q

Blood vessels contract to seal the wound or reduce the blood flow is called?

A

vasoconstriction

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21
Q

platelet plug is produced when?

A

Platelets become activated, adhere to the site of injury, secrete the contents of their gran- ules, and aggregate with other platelets to form a platelet plug.

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22
Q

_____ and _____ comprise the initial, rapid, short-lived response to vessel damage, but to control major bleeding in the long term, the plug must be reinforced by fibrin.

A

Vasoconstriction and platelet plug formation

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23
Q

Vasoconstriction and platelet plug formation comprise the initial, rapid, short-lived response to vessel damage, but to control major bleeding in the long term, the plug must be reinforced by?

A

Fibrin

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24
Q

Defects in primary hemostasis that can cause debilitating, sometimes fatal, chronic hemorrhage. (4)

A

collagen abnormalities, thrombocytopenia, qualitative platelet disorders, or von Willebrand disease

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25
Q

describes the activation of a series of coagulation proteins in the plasma, mostly serine proteases, to form a fibrin clot.

A

Secondary hemostasis

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26
Q

an enzyme that converts fibrinogen to a localized fibrin clot

A

thrombin

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27
Q

The final event of hemostasis is?

A

fibrinolysis, the gradual digestion and removal of the fibrin clot as healing occurs.

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28
Q

Activated by desquamation and small injuries to blood vessels

A

Primary hemostasis

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29
Q

Involves vascular intima and platelets

A

Primary hemostasis

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30
Q

Rapid, short-lived response

A

Primary hemostasis

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31
Q

Procoagulant substances exposed or released by damaged or activated endothelial cells

A

Primary hemostasis

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32
Q

Activated by large injuries to blood vessels and surrounding tissues

Involves platelets and coagulation system

Delayed, long-term response

The activator, tissue factor, is exposed on cell membranes

A

Secondary hemostasis

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33
Q

_____ provides the interface between circulating blood and the body tissues.

A

vascular intima

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34
Q

The innermost lining of blood vessels is a monolayer of metabolically ________

A

active endothelial cells

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35
Q

ECs play essential roles in?

A

immune response, vascular permeability, proliferation, and, of course, hemostasis.

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36
Q

______ form a smooth, unbroken surface that eases the fluid passage of blood.

A

Endothelial cells

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37
Q

An ____________ (basement membrane) and its surrounding layer of connec- tive tissues support the ECs.

A

elastin-rich internal elastic lamina

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38
Q

In all blood vessels, ________ occupy the connective tissue layer and produce collagen.

A

fibroblasts

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39
Q

Smooth muscle cells in ______ and _______, but not in the walls of veins, venules, or capillaries, contract during primary hemostasis.

A

arteries and arterioles

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40
Q

Normally, the intact _________ prevents thrombosis by inhibiting platelet aggregation, preventing coagulation acti- vation and propagation, and enhancing fibrinolysis

A

vascular endothelium

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41
Q

Innermost Vascular Lining

A

Endothelial cells (endothelium)

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42
Q

Supporting the Endothelial Cells

A

Internal elastic lamina composed of elastin and collagen

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43
Q

Subendothelial Connective Tissue

A

Collagen and fibroblasts in veins
Collagen, fibroblasts, and smooth muscle cells in arteries

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44
Q

a platelet inhibi- tor and a vasodilator, is synthesized through the eicosanoid pathway and prevents unnecessary or undesir- able platelet activation in intact vessels

A

Prostacyclin

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45
Q

is synthesized in ECs, vascular smooth muscle cells, neutro- phils, and macrophages.

induces smooth muscle relaxation and subsequent vasodilation, inhibits platelet ac- tivation, and promotes angiogenesis and healthy arteri- oles

A

Nitric oxide

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46
Q

An important EC-produced anticoagulant is ________, which controls activation of the tissue factor pathway, also called the extrinsic coagula- tion pathway.

A

tissue factor pathway inhibitor (TFPI)

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47
Q

ECs synthesize and express on their surfaces
inhibitors of thrombin formation, _______, facilitated by _________, and _______

A

thrombomodulin; endothelial protein C receptor (EPCR); heparan sulfate

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48
Q

______ binds protein C, and ______ catalyzes the activation of the protein C pathway

A

EPCR; thrombomodulin

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49
Q

downregulates coagulation by digesting activated factors V and VIII, thereby
inhibiting thrombin formation

A

protein C pathway

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50
Q

protein C pathway downregulates coagulation by digesting activated factors ____ and ____, thereby
inhibiting thrombin formation

A

V and VIII

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51
Q

is a glycosaminoglycan that
enhances the activity of antithrombin, a serine
protease inhibitor.

A

Heparan sulfate

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52
Q

a serine protease inhibitor.

A

Antothrombin

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53
Q

manufactured from porcine gut tissues, resembles EC heparan sulfate in its antithrombin activity

A

pharmaceutical anticoagulant heparin,

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54
Q

pharmaceutical anticoagulant heparin,
manufactured from _______ resembles EC heparan sulfate in its antithrombin
activity

A

porcine gut tissues

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55
Q

is used extensively as a therapeutic
agent to prevent propagation of he thrombi that cause coronary thrombosis, strokes, deep vein thromboses, and pulmonary emboli

A

Heparin

56
Q

ECs secrete _______ from storage sites called Weibel-Palade bodies when activated by vasoactive agents such as thrombin

A

Von Willebrand factor (VWF)

57
Q

ECs secrete von Willebrand factor (VWF) from storage sites called _______ when activated by vasoactive agents such as thrombin

A

Weibel-Palade bodies

58
Q

ECs secrete and coat themselves with ______, an adhesion molecule that promotes platelet and leukocyte binding

A

P-selectin

59
Q

ECs support ______ (secretion of tissue plasminogen activator (TPA))

A

fibrinolysis

60
Q

Activates plasminogen to form plasmin

A

Tissue plasminogen activator (TPA)

61
Q

thrombus formation

A

both TPA and plasminogen bind to polymerized fibrin

62
Q

TPA activates fibrinolysis by?

A

converting plasminogen to plasmin

63
Q

from the cytoplasm of bone marrow megakaryocytes

A

Platelets

64
Q

Platelets are from the cytoplasm of ______

A

bone marrow megakaryocytes

65
Q

PLATELETS size

A

2 to 3 um in diameter

66
Q

complex, metabolically active cells that interact
with their environment and initiate and control hemostasis platelets adhere, aggregate, and secrete the contents of their granules (during injury)

A

Platelets

67
Q

is the property by which platelets bind nonplatelet surfaces such as subendothelial collagen

A

Adhesion

68
Q

platelet adhesion is underscored by bleeding disorders such as

A

Bernard-Soulier syndrome

69
Q

What are the platelet factors absent in Bernard-Soulier syndrome

A

platelet GP Ib/IX/V

70
Q

Platelets functions (3)

A

Adhesion
Aggregation
Secretion

71
Q

What condition where the VWF is missing or defective.

A

von Willebrand disease

72
Q

Platelet a-Granules: ______ molecules (7)

A

Factor V
Factor XI
Protein S
Fibrinogen
VWF
Platelet factor 4 (heparin inhibitor)
Platelet-derived growth factor

73
Q

Platelet Dense Granules (Dense Bodies) (3)

A

Adenosine triphosphate
Calcium
Serotonin (vasoconstrictor)

74
Q

Plasma transports at least ____ procoagulants (COAGULATION FACTORS)

A

16

75
Q

Procoagulants is also termed as

A

Coagulation Factor

76
Q

_____ are enzymes that circulate in an inactive form called ______

A

8; zymogens

77
Q

____ that bind, stabilize, and enhance the activity of their respective enzymes

A

cofactors

78
Q

glycoproteins synthesized in the?

A

Liver

79
Q

During clotting - procoagulants become
activated and produce a _____

A

localized thrombus

80
Q

What are the zymogens? (8)

A

VII
IX
X
XI
XII
XIII
Prekllikrein
Prothrombin

81
Q

Cofactors (7)

A

V
VIII
HMWK
Protein Z
Protein S
Tissue factor
Thrombomodulin

82
Q

The plasma procoagulants may be serine proteases or cofactors, except for factor _____, which is a transglutaminase

A

XIII

83
Q

The plasma procoagulants may be _____ or _____ except for factor XIII, which is a transglutaminase

A

Serine proteases or cofactors

84
Q

The plasma procoagulants may be serine proteases or cofactors, except for factor XIII, which is a ?

A

transglutaminase

85
Q

Serine proteases are proteolytic enzymes of the trypsin family and include the procoagulants (7)

A

factor Ila (thrombin)
VIla
IXa
Xa
Xla
XIla
pre-K

86
Q

Also known as fletcher factor

A

Pre-kallikrein

87
Q

is the ultimate substrate of the coagulation pathway

A

Fibrinogen

88
Q

is required for the assembly of coagulation complexes on platelet or cell membrane phospholipids

A

Calcium

89
Q

Factor I : Name & Function

A

Fibrinogen

Thrombin substrate, polymerizes to form fibrin

90
Q

Factor II : Name & Function

A

Prothrombin

Serine protease

91
Q

Factor III: Name & Function

A

Tissue factor

Cofactor

92
Q

Factor IV: Name & Function

A

Ionic calcium

Mineral

93
Q

Factor V: Name & Function

A

Labile factor

Cofactor

94
Q

Factor VII: Name & Function

A

Stable factor

Serine protease

95
Q

Factor VIII: Name & Function

A

Antihemophilic factor

Cofactor

96
Q

Factor VWF: Name & Function

A

von Willebrand factor

Factor VIII carrier and platelet adhesion

97
Q

Factor IX: Name & Function

A

Christmas factor

Serine protease

98
Q

Factor X: Name & Function

A

Stuart-Prower factor

Serine protease

99
Q

Factor XI: Name & Function

A

Plasma thromboplastin antecedent (PTA)

Serine protease

100
Q

Factor XII: Name & Function

A

Hageman factor

Serine Protease

101
Q

Factor Prekallikrein : Name & Function

A

Fletcher factor, pre-K

Serine protease

102
Q

Factor High-molecular- weight kininogen: Name & Function

A

Fitzgerald factor, HMWK

Cofactor

103
Q

Factor XIII: Name & Function

A

Fibrin-stabilizing factor (FSF)

Transglutaminase, transamidase

104
Q

Platelet factor 3: Name & Function

A

Phospholipids, phosphatidyl- serine, PF3

Assembly molecule

105
Q

Other plasma coagulant

A

Fibrinogen
Factor XIII
Phospholipids
Calcium VWF

106
Q

is a transmembrane receptor for factor VIlla and is found on extravascular cells such as fibroblasts and smooth muscle cells, but under normal conditions, it is not found on blood vessel ECs.

A

Tissue factor (factor III)

107
Q

are soluble plasma proteins. Both are activated by thrombin and inactivated by protein C

A

Factors V and VIII

108
Q

Factors V and VIII are soluble plasma proteins. Both are activated by ____ and inactivated by _____

A

thrombin; protein C

109
Q

________ is a cofactor to factor XIla and prekallikrein in the intrinsic contact factor complex.

A

High-molecular-weight kininogen

110
Q

High-molecular-weight kininogen is a cofactor to factor ____ and _____ in the intrinsic contact factor complex

A

XIla; prekallikrein

111
Q

a mechanism for activating coagulation in conditions where foreign objects such as mechanical heart valves or bacterial membranes and/or high levels of inflammation are present

A

intrinsic contact factor complex

112
Q

a transmembrane protein constitutively expressed by vascular ECs, is a thrombin cofactor.

A

Thrombomodulin

113
Q

Both ______ and _____are cofactors in the regulation and control of coagulation

A

protein S and protein C

114
Q

Factor VIII has a molecular mass of 260,000 Daltons and is produced primarily by?

A

Hepatocytes

115
Q

_______ and ________ are therefore sex-linked disorders occur- ring almost exclusively in males

A

Hemophilia A and Hemophilia B

116
Q

What is the condition for factor VIll deficiency

A

Hemophilia A

117
Q

What is the condition for factor IX deficiency

A

Hemophilia B

118
Q

______ is a cofactor, but its importance in hemostasis cannot be overstated, as evidenced by the severe bleeding and symptoms associated with hemophilia A

A

Factor VIII

119
Q

_______ deteriorates more rapidly than the other coagulation factors in stored blood

A

Factor VIII

120
Q

______ is a large multimeric glycoprotein that participates in platelet adhesion and transports the procoagulant factor VIII

A

VWF

121
Q

“contact factors”, also called intrinsic accessory pathway proteins, are factors (3)

A

factor XIl, high-molecular- weight kininogen (HMWK, factor), and prekallikrein (pre-K, Fletcher factor)

122
Q

Contact factors are AKA

A

intrinsic accessory pathway proteins

123
Q

The contact factor complex (HMWK:pre-K.FXII) activates factor _____; factor Xla is an activator of factor _____

A

XI; IX

124
Q

True or false: Deficiencies of factor XII, HMWK, or pre-K do not cause clinical bleeding disorders.

A

True

125
Q

______ is activated by the contact factor complex and, more significantly, by ______ during coagulation generated from tissue factor activation

A

Factor XI; thrombin

126
Q

What do you call the Deficiencies of factor XI

A

Rosenthal syndrome

127
Q

Deficiencies of factor XI (Rosenthal syndrome) usually result in?

A

mild and variable bleeding

128
Q

cleave fibrinopeptides A and B from the alpha and beta chains of the fibrinogen molecule, triggering spontaneous fibrin polymerization

A

Thrombin

129
Q

In addition, thrombin amplifies the coagulation mechanism by activating cofactors?

A

V, VIII, XI

130
Q

In addition, thrombin amplifies the coagulation mechanism by activating cofactors V and VIII and factor XI by a?

A

positive feed- back mechanism

131
Q

Thrombin can also activate factor?

A

VIII

132
Q

is the primary substrate of thrombin

A

Fibrinogen

133
Q

essential for platelet aggregation because it links activated platelets through their GP IIb/Illa platelet fibrinogen receptor.

A

Fibrinogen

134
Q

an acute phase reactant protein

A

Fibrinogen

135
Q

two coagulation pathways were described, both of which activated ________ at the start of a common pathway leading to thrombin generation

A

factor X

Finals (20 decks)

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