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CV Test 4 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

The stages of hemostasis?

A

Primary
Secondary
Fibrinolysis

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2
Q

What is primary hemostasis?

A

Formation of the platelet plug

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3
Q

What is secondary hemostasis?

A

Coagulation

When the actual clot forms

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4
Q

What is fibrinolysis?

A

Clot is dissolved

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5
Q

What is the vessel itself’s initial response to injury?

A

Vasospasm

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6
Q

What stimulates the vasospasm of the injured vessel to occur?

A

Disrupted endothelium

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7
Q

What stage includes formation of the platelet plug?

A

Primary

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8
Q

What initiates formation of the platelet plug?

A

Injury to vessel exposes endothelial collagen

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9
Q

What coagulation factor is required for adhesion of platelets?

A

Von Wilebrand

vW

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10
Q

What factor(s) activate platelets for the platelet plug?

A

Thrombin and tissue factor

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11
Q

What is meant by platelet activation?

A

Platelets change shape

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12
Q

What prostaglandin promotes platelet aggregation?

A

Thromboxane

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13
Q

What substances are also included in the platelet plug?

A

Fibrinogen and thrombin

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14
Q

Aggregation of platelets triggers further?

A

Attraction of more platelets

Platelet activation

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15
Q

What kind of bleeding/injury do platelet plugs control?

A

Minute vessel breaks that occur constantly

-full clot not required

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16
Q

Platelet counts under what allow spontaneous bleeding to occur?

A

< 20,000

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17
Q

Intercerebral hemorrhage can occur from just a platelet count below?

A

< 20,000

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18
Q

Thrombocytopenia means what? And what can you see with this as evidence of someone unable to form platelet plugs?

A

Low platelet count

Petechia

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19
Q

Production of thromboxane requires what?

A

Cyclooxygenase (COX)

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20
Q

What inhibits the production of the prostaglandin thromboxane?

A

Cox inhibitors interferes with the enzyme cyclooxygenase, which means it interferes with the production of thromboxane

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21
Q

COX inhibitors interfere with what part of hemostasis?

A

Function of the platelets

  • platelet aggregation
  • formation of a platelet plug
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22
Q

What COX inhibitor has temporary interference on hemostasis?

A

NSAIDs

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23
Q

How long do NSAIDs interfere with platelet function?

A

1-2 days

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24
Q

What cox inhibitor has permanent interference on platelet function?

A

Aspirin

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25
Q

Why is ASA interference considered permanent?

A

It lasts the life of a platelet

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26
Q

What is the life of a platelet?

A

8-12 days

-1-2 weeks

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27
Q

How long does ASA interfere with platelet function?

A

1-2 weeks

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28
Q

What lab tests will tell platelet function, NOT count?

A

Bleeding time

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29
Q

What bleeding time may indicate bleeding risk?

A

Over 7-8 minutes

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30
Q

What platelet count constitutes thrombocytopenia?

A

< 100,000

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31
Q

What platelet count constitutes surgical bleeding risk?

A

< 50,000

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32
Q

What platelet count constitutes spontaneous bleeding?

A

< 20,000

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33
Q

What are the 4 A’s of platelet plug?

A

Activation
Adhesion
Aggregation
Attraction

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34
Q

What changes the platelet plug into a clot?

A

Fibrin

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35
Q

What is the inactive form of fibrin?

A

Fibrinogen

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36
Q

What factor converts fibrinogen into fibrin?

A

Thrombin

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37
Q

What is the inactive form of thrombin?

A

Prothrombin

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38
Q

What factor converts prothrombin into thrombin?

A

Factor X

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39
Q

What constitutes the chain of events that occur from factor X > fibrin formation?

A

The common pathway

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40
Q

The formation of fibrin requires what substances?

A

Fibrinogen
Calcium
Thrombin

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41
Q

The formation of thrombin requires what substances?

A

Prothrombin
Calcium
Factor X

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42
Q

What (old) 2 pathways were described to get to factor X?

A

Extrinsic and Intrinsic pathway

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43
Q

What factors are involved in the extrinsic pathway and what lab test would show abnormalities?

A

III
VII
PT

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44
Q

What factors are involved in the intrinsic pathway and what lab test would show abnormalities?

A 
VIII
IX
XI
XII
PTT
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45
Q

What has replaced the intrinsic/extrinsic pathways?

A

The cell based theory

-tissue factor theory

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46
Q

What factor does the cell based theory say triggers coagulation?

A

Factor III

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47
Q

What are the many names for factor III?

A

Tissue factor
Thromboplastin
Tissue thromboplastin

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48
Q

What are the phases of cell based theory?

A

Initiation
Amplification
Propagation

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49
Q

Describe initiation phase

A

Triggered by vessel injury to endothelial surface exposing tissue factor
Tissue factor and factor VII activate factor X

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50
Q

How much thrombin is created due to initiation phase

A

Only a small amount

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51
Q

Describe the amplification phase

A

XXX

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52
Q

How much thrombin is created from the activation stage?

A

Thrombin generation is gaining momentum

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53
Q

Describe the propagation phase

A

XXXX

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54
Q

This propagation phase is also the?

A

The common pathway

55
Q

What is thromboelastogram?

A

Lab test: TEG

-follows clot through initiation, complete formation, strength and lysis

56
Q

What can TEG not detect?

A

vW disease or ASA effects

57
Q

What is the R time on TEG?

A

Time to begin forming clot

58
Q

What is the problem if R is prolonged in a TEG?

A

Coagulation factors

59
Q

What is the K describe on a TEG?

A

Time of clot strengthening

60
Q

What is the problem if K is prolonged on TEG?

A

Fibrinogen

61
Q

What is MA on a TEG?

A

Measures the clot’s strength

62
Q

What is the problem in the MA on a TEG?

A

Platelets

63
Q

What is the determined by the time period after the MA?

A

Fibrinolysis

64
Q

TEG waveforms

A

TEG waveforms

65
Q

What is responsible for clot lysis?

A

Plasmin

66
Q

How does plasmin dissolve the clot?

A

It removes the fibrin

67
Q

What activates the plasminogen?

A

Tissue plasminogen activator

-tPA

68
Q

What inhibits plasmin?

A

Anti plasmin

-supports clot

69
Q

What class of drugs dissolve clots?

A

Thrombolytics

70
Q

Name 3 plasminogen activators

A

TPA and analogues
Streptokinase
Urokinase

71
Q

Name 3 plasmin inhibitors

A

Aprotinin
Amicar amiocarproic acid
Transexamic acid

72
Q

What is the most common inherited bleeding disorder?

A

VonWillebrands disease

73
Q

What is vonWillebrand’s needed for?

A

Adhesion of platelets

74
Q

What medication can exacerbate vW symptoms?

A

ASA

-should be avoided

75
Q

What lab results are seen with vW?

A

Prolonged bleeding time
PT/PTT may be normal
PLT count may also be normal

76
Q

What is the first line treatment for vW? Why?

A

DDAVP

It treats the most common form of vW

77
Q

What is DDAVP?

A

Analogue of vasopressin

78
Q

What is given if vW patient does not respond to DDAVP?

A

FFP

Non-recombinant factor VIII

79
Q

Why must non-recombinant factor VIII be used?

A

Recombinant factor VIII is artificially created and does not contain vW

80
Q

Where is factor VIII made?

A

In the liver

81
Q

Where is vW synthesized?

A

By vessel endothelial cells

82
Q

What is the relationship between vW and factor VIII?

A

vW with factor VIII combine to take part in coagulation

-VIIIc is without vW

83
Q

Hemophilia is an abnormality on which chromosome?

A

X

84
Q

What lab value would show hemophilia?

A

Prolonged PTT

85
Q

What is hemophilia A?

A

Deficiency of factor VIIIc

-treatment is factor VIII

86
Q

What is hemophilia B?

A

Deficiency of factor IX

87
Q

What can treat both types of hemophilia?

A

FFP

88
Q

What type of hemophilia can cryoprecipitate treat?

A

Hemophilia A

-though controversial

89
Q

Which type of hemophilia is more common?

A

Hemophilia A

90
Q

What is the most common inherited defect in secondary hemostasis?

A

Hemophilia A

91
Q

What is the most common inherited cause of abnormal bleeding?

A

VW disease

92
Q

What is the most common inherited cause of abnormal secondary coagulation?

A

Hemophilia A

93
Q

What is the most common cause of abnormal bleeding?

A

ASA

94
Q

What is more common acquired bleeding problem or inherited?

A

Acquired

95
Q

What are examples of acquired bleeding problems?

A 
Liver disease
Decreased function VIII, IX, XI
RA
Colitis
Aging
Systemic lupus erythematous
96
Q

What factors are NOT made by the liver?

A

VW: endothelium
Calcium: factor IV from diet
III: from damaged tissue

97
Q

Liver disease causes what lab abnormalities?

A

Elevated PT and PTT

98
Q

Vitamin K is required for the liver to synthesize what factors?

A

II
VII
IX
X

99
Q

What contains all coagulation factors except platelets?

A

FFP

100
Q

What does FFP also contain?

A

Anticoagulation factors like antithrombin III

101
Q

What is in cryoprecipitate?

A

Factor VIII
Fibrinogen
XIII

102
Q

What is stored banked blood deficient in?

A

Platelets
Factor V
Factor VIII

103
Q

What factor has the shortest half life?

A

Factor VII

104
Q

Why does stored banked blood has deficiencies?

A

Because of the process of removing the plasma

105
Q

What is dilutional coagulopathy?

A

So much banked blood has been giving which doesn’t have factors V, VIII and platelets

106
Q

What is usually the biggest problem with dilutional coagulopathy?

A

Low platelets

107
Q

Platelets may be need if how much banked blood has been given?

A

10-15 units

108
Q

With dilutional coagulopathy a patient’s factors have to fall below what % for coagulation to no longer be normal?

A

< 30%

109
Q

What can be given with dilutional coagulopathy after platelet transfusion and bleeding still a problem?

A

FFP

110
Q

Name some anti-coag factors

A

Antithrombin (antithrombin III)
Protein S
Protein C
Thrombomodulin

111
Q

What drug class inhibits further clot formation?

A

Anticoagulants

112
Q

What does Heparin augment?

A

Antithrombin III

113
Q

Heparin interferes with which pathway?

A

Intrinsic

114
Q

So what factors are affected by Heparin?

A 
I
II
V
VIII
IX
X
XI
XII
By interfering with intrinsic pathway, it also interferes with the common pathway
115
Q

How is the activity of Heparin monitored?

A

PTT

116
Q

What explains heparin resistance?

A

Low antithrombin III

117
Q

How is low antithrombin III treated?

A

FFP

-so heparin resistance is treated with FFP

118
Q

What is the most common cause of drug induced thrombocytopenia?

A

Heparin Induced Thrombocytopenia (HIT)

119
Q

What is a risk of using direct thrombin inhibitors?

A

Increased risk of bleeding

-it can not be reversed

120
Q

Name direct thrombin inhibitors

A

Bivalirudin
Argatroban
Hirudin
Dabigatran

121
Q

What direct thrombin inhibitor has the shortest half life?

A

Bivalirudin

122
Q

Name direct factor X inhibitors

A

Fondaparinux
Rivaroxaban
Apixaban

123
Q

What are the advantages of low molecular weight heparin?

A 
Longer half life
More predictable
Less monitoring needed
Less platelet inhibition
Less HIT
124
Q

What are the disadvantages of LMWHeparin?

A

Not reversible

125
Q

How does Coumadin work?

A

Competes with vitamin K at the liver

126
Q

What factors are affected by this vitamin K competition with Coumadin?

A

II
VII
IX
X

127
Q

What pathway does Coumadin interfere with?

A

Extrinsic pathway

128
Q

What test does Coumadin affect?

A

PT

129
Q

What test is Coumadin monitored for therapeutic levels?

A

INR

-ratio that tells you how much longer clotting takes

130
Q

What is disseminated intravascular coagulation?

A

Uncontrolled coagulation activation
Widespread thrombosis of small vessels
Consumes clotting factors and platelets

131
Q

What type of things can DIC be a secondary complication of?

A 
Sepsis
Shock
Post op
Transfusion reaction
OB complications
Others
132
Q

What are the symptoms of DIC?

A 
Spontaneous diffuse hemorrhage
Decreased platelets
Decreased fibrinogen
Elevated PT
Elevated PTT
Elevated fibrin degradation products
133
Q

What is the distinctive characteristic of DIC? (2 names)

A

Elevated fibrin degradation products

AKA fibrin split products

134
Q

What is the treatment of DIC?

A

Platelets and FFP
Treat underlying cause
Heparin is a controversial treatment

CV Test 4 (2 decks)

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