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FLUIDS-Coagulation Flashcards

1
Q

Describe the difference in artery and vein anatomy

A
  1. Tunica media is thicker in arteries
  2. Tunica externa is the thickest layer in veins
  3. The tunica externa is thinner than tunica media
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2
Q

What are the 3 layers of arteries and veins from outer to inner

A
  1. Tunica externa (connective tissue)
  2. Tunica media (smooth muscle layer and elastic tissue)
  3. Tunica intima (endotherlium)
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3
Q

4 factors that contribute to the liquid state of blood

A
  1. Coagulation proteins circulate in inactive form
  2. Endothelium is smooth, repelling clotting factors
  3. Undamaged endothelium prevents activation of platelets
  4. Activated factors are removed by brisk blood flow
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4
Q

What are the 4 steps of hemostasis

A
  1. Vascular spasm
  2. Formation of the platelet plug (primary hemostasis)
  3. Coagulation and fibrin formation (secondary hemostasis)
  4. Fibrinolysis when clot is no longer needed
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5
Q

What can over abundance of procoagulants increase the risk of

A
  1. Stroke
  2. MI
  3. Thrombosis
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6
Q

What 2 processes favor clot formation in the body

A
  1. Procoagulation

2. Antifibrinolysis

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7
Q

What 2 factors favor the prevention or destruction of clots

A
  1. Anticoagulation

2. Fibrinolysis

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8
Q

What are 5 procoagulant substances

A
  1. Coagulation factors
  2. Collagen
  3. wVF
  4. Fibronectin
  5. Thrombomodulin
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9
Q

What are 4 native anticoagulant substances

A
  1. Protein C
  2. Protein S
  3. Antithrombin
  4. Tissue pathway factor inhibitor
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10
Q

What are 3 native fibrinolytic substances

A
  1. Plasminogen
  2. tPA
  3. Urokinase
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11
Q

What are 2 native antifibrinolytic substances

A
  1. Alpha-antiplasmin

2. Plasminogen activator inhibitor

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12
Q

What are 2 native vasoconstriction mediators

A
  1. Thromboxane A2
  2. ADP
  3. Serotonin
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13
Q

What are 2 native vasodilation mediators

A
  1. Nitric oxide

2. Prostacyclin

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14
Q 
What are the functions of the following
Coagulation factor=
Collagen=
wVF=
Fibronectin=
Thrombomodulin=
A 
Procoagulants
Coagulation factor= coagulation
Collagen= Tensile strength
wVF= Plt adhesion
Fibronectin= Cell adhesion
Thrombomodulin= Regulates naturally occurring anticoags
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15
Q 
What are the functions of the following
Protein C=
Protein S=
Antithrombin=
Tissue pathway factor inhibitor=
A

Anticoagulants
Protein C= degrades factor 5a and 8a
Protein S= Cofactor for protein C
Antithrombin= Degrades factor 9a, 10a, 11a, 12a
Tissue pathway factor inhibitor= inhibits tissue factor

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16
Q

What are the functions of the following
Plasminogen=
tPA=
Urokinase=

A

Fibrinolytics
Plasminogen= Precursor to plasmin (breaks down fibrin)
tPA= activates plasmin
Urokinase= activates plasmin

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17
Q

What are the functions of the following
Alpha-antiplasmin=
plasminogen activator inhibitor=

A

Antifibrinolytics
Alpha-antiplasmin= inactivates tPA, urokinase
plasminogen activator inhibitor= Inhibits plasmin

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18
Q

How are platelets produced

A

Megakaryocytes in the bone marrow

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19
Q

Normal platelet level

A

150,000 - 300,000mm^3

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20
Q

What is the lifespan of the platelet

A

8-12 days (1-2 weeks)

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21
Q

How are platelets cleared

A

By macrophages in the reticuloendothelial system of the spleen

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22
Q

How does the spleen affect platelet levels

A
  1. It clears them via macrophages in the reticuloendothelial system
  2. Can sequester up to 1/3 of all circulating platelets
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23
Q

Where are up to 1/3 of platelets stored

A

Spleen

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24
Q

What are 2 essential functions of the platelet

A
  1. Structural component of the clot

2. Delivery vehicles providing many substates required for clot formation

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25
Q

What components are on the external membrane of the platelet

A
  1. Glycoproteins

Phospholipids

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26
Q

What is the function of glycoproteins on the platelet external membrane

A
  1. Repellant of healthy vascular endothelium

2. Adheres to injured endothelium, collagen, and fibrinogen

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27
Q

What 3 components can the glycoprotein of the platelet membrane adhere

A
  1. Endothelium
  2. Collagen
  3. Fibrinogen
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28
Q

How does the platelet membrane glycoprotein adhere to injured structures

A
  1. GpIb attaches to activated platelet to vWF

2. GpIIb-IIIa complex links platelets together to form plug

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29
Q

How are platelets linked to form a plug

A

GpIIb-IIIa complex links the platelets together

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30
Q

What is the function of platelet membrane phopholipids

A

It’s a substrate for prostaglandin synthesis

-Which produces thromboxane A2

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31
Q

What is the function of thromboxane A2

A

Platelet activation

A platelet which has synthesized prostaglandin can then activate other platelets

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32
Q

What are 7 internal platelet components

A
  1. Actin and myosin
  2. Thrombosthenin
  3. ADP
  4. Calcium
  5. Fibrin-stabilizing factor
  6. Serotonin
  7. Growth factor
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33
Q 
What are the functions or the following internal platelet components
Actin/Myosin=
Thrombosthenin=
ADP=
Calcium=
Fibrin-stabilizing factor=
Serotonin=
Growth factor=
A

Actin/Myosin= plt contraction to form plug
Thrombosthenin= plt contraction assist
ADP= Plt activation and aggregation
Calcium= Coag cascade Fx 4
Fibrin-stabilizing factor= Crosslinks fibrin (Fx 13)
Serotonin= Activates nearby plts
Growth factor= Repair damaged vessel wal

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34
Q

What 2 components that are contained inside the plt aid in platelet contraction

A
  1. Actin and myosin

2. Thrombosthenin

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35
Q

What 2 components that are contained inside the plt aid in plt activation

A
  1. ADP

2. Serotonin

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36
Q

How does undamaged endothelium prevent platelet function

A

By secreting

  1. Prostaglandin I2
  2. Nitric oxide
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37
Q

What are 3 functions of prostaglandin I2 and where is it secreted

A

Secreted by healthy endothelium

Inhibits plt function by

  1. preventing vWF adherence
  2. TxA2 activation on plt
  3. release of storage granules
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38
Q

How does nitric oxide prevent platelet function

A

It inhibits TxA2 receptor on the plt

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39
Q

What are 5 platelet surface receptors

A
  1. GPIb
  2. ADP
  3. TxA2
  4. Thrombin
  5. GPIIb-IIIa
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40
Q

What 3 actions are responsible for the contraction of injured vessels

A
  1. SNS reflex
  2. Myogenic response
  3. Release of vasoactive substances (TxA2)
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41
Q

What is the purpose of vascular spasm following injury

A
  1. reduces blood loss

2. Helps procoagulatns remain in affected area

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42
Q

What is primary homeostasis, including the 3 step-process

A

Formation of platelet plug via

  1. Adhesion
  2. Activation
  3. Aggregation
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43
Q

What 2 actions occur during primary homeostasis adhesion

A
  1. Collagen is exposed and plts adhere via Gp Ia/IIa and Gp VI receptors
  2. vWF is synthesized and released to bind with GpIb receptor
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44
Q

What is the function of vWF

A

ADHESION

to bind with GpIb receptor on the plt and anchor it to the subendothelium

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45
Q

What is Von willebrand disease

A

A disorder of plt adhesion

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46
Q

How are platelets activated during primary homeostasis

A

Expose collagen and thrombin activate the plts

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47
Q

What happens once plts are activated by collagen and thrombin

A

Plts release ADP and thromboxane A2 which activate nearby plts

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48
Q

How are nearby plts activated

A

The original plt releases ADP and thromboxane A2

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49
Q

Which substance released by the plt can aid in vasoconstriction

A

TxA2

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50
Q

What does plt contraction do (3)

A
  1. Promotes plt plug
  2. Releases alpha granules (fibrinogen, fibronectin, vWF, plt Fx 4, plt growth factor)
  3. Recruits other plts to injured site
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51
Q

What are 2 glycoproteins that are expressed on an activated plt

A

GpIIb and GpIIIa

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52
Q

How is plt aggregation accomplished

A

GpIIb/IIIa receptor complex links activated plt to form plug

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53
Q

What factors are required to help configure GpIIb/IIIa to accept fibrinogen

A

TxA2 and ADP

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54
Q

What is the primary purpose of the coagulation cascade

A

To produce firbin

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55
Q

When is the coagulation cascade not necessary

A

When injury is minimal and only plt plug is needed

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56
Q

What is the different events that initiate the extrinsic vs intrinsic pathway

A

Extrinsic = when coagulation is initiated outside of the intravascular space

Intrinsic = When coagulation is initiated inside the intravascular space

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57
Q

What is a mnemonic for coagulation factors

A

Foolish People Try Climbing Long Slopes After Christmas Some People Have Fallen

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58
Q

What are the coagulation factors in order

A
  1. Fibrinogen
  2. Prothrombin
  3. Tissue factor
  4. Calcium ions
  5. Labile factor
  6. Stable factor
  7. Antihemophilic factor
  8. Christmas factor
  9. Stuart-Power factor
  10. Plasma thromboplastin antecedent
  11. Hageman factor
  12. Fibrin stabilizing factor
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59
Q

Where are the coagulation factors synthesized

A

Diet = Fx 4
Vascular wall = Tissue factor (Fx 3)
Liver = all other factors

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60
Q

Which factors are vitamin k dependent

A

Fx 2, 7, 9, 10

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61
Q

Which clotting factors are co-factors

A

5 and 8

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62
Q

Which clotting factor begins the common pathway

A

Fx 10

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63
Q

Which clotting factor initiates the extrinsic path

A

TF (Fx 3)

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64
Q

Which clotting factor initiates the intrinsic path

A

Fx 12

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65
Q

What labs measure the intrinsic vs extrinsic path

A 
Intrinsic = PTT, ACT
Extrinsic = PT, INR
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66
Q

Which factors are part of the common pathway

A

10, (5), 2, 1

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67
Q

Which factors are part of the intrinsic pathway

A

12, 11, 9, (8)

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68
Q

Which factors are part of the extrinsic path

A

TF/Fx3, 7, 4

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69
Q

Which anticoagulant inhibits the extrinsic pathway

A

Warfarin

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70
Q

How does Fx 7 activate Fx 10

A

Requires Fx 4 (calcium)

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71
Q

What is the purpose of Fx 5

A

In the common pathway, it functions in a positive feedback role that accelerates production of prothrombin activator

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72
Q

How is Fx 2 (prothrombin to thrombin) activated

A

By prothrombin activator and plt phospholipids

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73
Q

Which clotting factor has the shortest half-life.

Why is this significant

A

Fx 7 (4-6 hrs)

Significance = first factor to become deficient in pts with liver failure, vitamin K deficiency, and taking warfarin

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74
Q

What is the first factor to be depleted in pts with liver failure, vit K deficiency or taking warfarin

A

Fx 7

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75
Q

What activates Fx 12

A

Blood trauma, and exposure to collagen

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76
Q

What activates Fx 11

A

Fx 12a

Requires HMW kininogen and accelerated by prekalikrein

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77
Q

What activates Fx 9

A

Fx 11a

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78
Q

What activates Fx 10

A

Fx 9a and 8

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79
Q

What factor is missing with hemophilia A

A

Fx 8

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80
Q

What is the mnemonic for the extrinsic path

A

For 37 cents, you can purchase the extrinsic pathway

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81
Q

What is the mnemonic for the intrinsic path

A

If you can’t buy the intrinsic path for $12, you can buy it for $11.98

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82
Q

What is the mnemonic to remember the common pathway

A

The final common path can be purchased at the five (5) and dime (10) for 1 or 2 dollars on the 13th month

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83
Q

What is the primary goal of the extrinsic or intrinsic pathway

A

To produce prothrombin activator, which initiates the common pathway by activated Fx 2 to 2a (thrombin)

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84
Q

What is the function of thrombin (2a)

A

It’s a proteolytic enzyme that changes fibrinogen to fibrinogen monomer

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85
Q

How is fibrin incorporated into the plt plug

A

Activated fibrin-stabilizing factor (13a) facilitates cross-linkage of fibrin fibers and completes the clot

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86
Q

What factor is required to complete fibrin activation and cross-link

A

Fx 13a and Fx 4(Ca++)

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87
Q

What are 4 mechanisms the body uses to prevent indefinite clot formation

A
  1. Vasodilation and washout ADP and TxA2
  2. Antithrombin inactivates thrombin (2a) and Fx 9a-12a
  3. Tissue factor path inhibitor neutralizes tissue factor
  4. Protein C and S inhibit Fx 5a and 8a
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88
Q

What is the role of antithrombin

A

Inactivates thrombin 2a and Fx 9a-12a

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89
Q

What is the role of tissue factor path inhibitor

A

Neutralizes tissue factor (3a)

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90
Q

What is the role of Protein C and S

A

Inhibition of Fx 5a and 8a

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91
Q

Where is plasminogen synthesized

A

The liver

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92
Q

What is plasmin

A

A proteolytic enzyme the degrades fibrin into fibrin degradation products

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93
Q

What lab measures fibrin degradation

A

D-Dimer

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94
Q

How is plasminogen activated

A

Injured tissue releases tissue plasminogen activator (tPA)

Plasminogen is incorporated into the clot and is dormant until it is activated

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95
Q

Where are the following released
tPA=
Urokinase=
Streptokinase=

A 
tPA= Injured tissue
Urokinase= produced and released by kidneys
Streptokinase= Streptococci secretion
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96
Q

What is the clinical use of plasmin activators

A

Dissolve thrombi and restore blood flow

97
Q

How is fibrinolysis terminated when no longer needed

A

tPA inhibitor = inhibits conversion of plasminogen to plasmin
Alpha-2 antiplasmin = inhibits action of plasmin on fibrin

98
Q

What are 2 enzymes that convert plasminogen to plasmin

A

tPA

Urokinase

99
Q

What are the 3 phases of the cell-based coagulation cascade

A
  1. Initiation
  2. Amplification
  3. Propagation
100
Q

What is the initiation phase of the cell-based coagulation cascade

A

When TF is expressed, the TF/7a reaction activates factor 10 (common path) making a small amount of thrombin (2a)

101
Q

What is the amplification phase of the cell-based coagulation cascade

A

Plt and cofactors amplify large-scale thrombin production

Activation of plts, Fx 5, and 11

102
Q

What is the propagation phase of the cell-based coagulation cascade

A

Large quantities of thrombin are produced on the surfaces of plts

103
Q

How does the propagation phase begin

A

When Fx 10 is activated by Fx 4 (Ca++), 8, and 9 on the surface of the plt

104
Q

What is the end-result of the propagation phase

A

The phase produces a positive feedback mechanism the produces enough thrombin to activate fibrin

105
Q

Why do thrombin levels remain low in the initiation phase of the cell-based coagulation cascade

A

Tissue factor pathway inhibitor (TFPI) limits the amount of tissue factor released

106
Q

What phase are plts activated in the contemporary coagulation model

A

The amplification phase

107
Q

What does aPTT measure

A

activated partial thromboplastin time
Intrinsic and final common pathways
The time it takes to form a clot using phospholipid and cCa++

108
Q

Normal PTT value

A

25-32 seconds

109
Q

How reduced are clotting factors before a change is seen with aPTT

A

by more than 30%

110
Q

What does PT measure

A

Prothrombin time
Measures the extrinsic and final common pathway

Time it take to form a clot using tissue factor and Ca++

111
Q

What does INR measure

A

Calculation that standardizes PT results

Ratio between pts PT and standard mean PT

112
Q

What is the normal INR and goal for pt s on warfarin

A

Normal = 1

On warfarin = 2-3

113
Q

What does the ACT measure and its purpose

A

Activated clotting time

Purpose = to guide heparin dosing

114
Q

What is normal ACT level

A

90-120 seconds

115
Q

What does a plt count NOT measure

A

The function of the plt, only the amount of plt

116
Q

What does bleeding time measure

A

Plt function

Evaluates the ability to form a plt plug

117
Q

What is a normal bleeding time

A

2-10 minutes

118
Q

What does a D-Dimer measure

A

Fibrinolysis

Elevated D-dimer = likely a thrombus somewhere in the body

119
Q

What are the 5 components of a TEG

A 
R time 
K Time
alpha angle
Max amplitude
Amplitude at minutes after MA
120
Q 
R Time: 
Definition=
Normal value=
Problem area=
Treatment=
A

Definition= Time to begin forming clot
Normal value= 6-8 min
Problem area= coagulation factors
Treatment= FFP

121
Q 
K Time: 
Definition=
Normal value=
Problem area=
Treatment=
A

Definition= Time until clot achieves fixed strength
Normal value= 3 - 7 min
Problem area= Fibrinogen
Treatment= Cryo

122
Q 
Alpha angle:
Definition=
Normal value=
Problem area=
Treatment=
A

Definition= Speed of fibrin accumulation
Normal value= 50-60 sec
Problem area= Fibrinogen
Treatment= Cryo

123
Q 
Max amplitude (MA):
Definition=
Normal value=
Problem area=
Treatment=
A

Definition= Measures clot strength
Normal value= 50-60 mm
Problem area= Platelets
Treatment= Plts, DDAVP

124
Q 
Amplitude at min after MA:
Definition=
Normal value=
Problem area=
Treatment=
A

Definition= Height of amplitude after 60 min
Normal value= MA - 5
Problem area= Excess fibrinolysis
Treatment= TXA, aminocaproic acid

125
Q

How is a prolonged TEG R time treated

126
Q

How is a prolonged K time treated

127
Q

How is a low alpha angle treated

128
Q

How is a low MA treated

129
Q

What 3 locations produce endogenous heparin

A

Basophils
Mast cells
Liver

130
Q

What pathway of coagulation cascade is affected by heparin

A

Intrinsic and final common pathway

131
Q

Heparin MOA

A

Binds to antithrombin forming a heparin-AT complex. This accelerates ATs anticoagulant ability

132
Q

What is the function of the heparin-AT complex

A

To neutralize thrombin (2a), and activated Fx 9-12

Inhibits plt function

133
Q

If heparinization has failed, what should be considered

A

AT deficiency

134
Q

Describe the properties of the heparin compound

A

Large, negatively charged, water-soluble compounds

Small Vd

135
Q

How is heparin metabolized

A

Heparinase

136
Q

How is heparin eliminated

A

Degradation by macrophages

Renal excretion

137
Q

What is the aPTT when heparin is therapeutic

A

1.5-2.5 normal ( 50-88 sec)

138
Q

When is ACT measured in conjunction with surgical heparin administration

A

Baseline (before heparin)
3 min post administration
Then q30 min

139
Q

What 3 physiologic factors affect ACT

A
  1. Hypothermia
  2. Thrombocytopenia
  3. Deficient fibrinogen, Fx 7 or Fx 12
140
Q

What are 5 side effects of heparin

A
  1. Hemorrhage
  2. HIT
  3. Allergic reaction
  4. HoTN
  5. Decreased AT concentration
141
Q

What are 3 contraindications for heparin use

A
  1. Neurosurgical procedures
  2. HIT
  3. Regional anesthesia (neuraxial)
142
Q

Describe the protamine compound

A

Highly alkaline

Strong positive charge

143
Q

What is the MOA of protamine

A

The positive charge of protamine and negative charge of heparin create a neutralization reaction that stops heparins activity

144
Q

Protamine dosing

A

1 mg for every 100 units of heparin in circulation

145
Q

How is the heparin-protamine complex cleared

A

Via the reticuloendothelial system

146
Q

What is unique about protamine administration alone

A

It is an anticoagulant

147
Q

What are 3 important side effects of protamine

A
  1. HoTN
  2. Pulmonary HTN
  3. Allergic reaction
148
Q

Why does HoTN occur with protamine administration and how is this attenuated

A

Histamine release

Give over >5 min

149
Q

Why can pulmonary HTN occur with protamine administration

A

TxA2 and serotonin release

150
Q

What can indicate a possible allergic reaction to protamine

A
  1. Fish allergy

2. Previous sensitization to NPH insulin

151
Q

What is warfarin MOA

A

Inhibition of the enzyme vitamin K epoxide complex. This complex converts inactive vit K to active vit K

152
Q

Which clotting factors are inhibited by warfarin and why

A

Fx 2, 7, 9, 10 b/c they are vit K dependent

Protein C and S

153
Q

Describe the protein binding ability of warfarin

A

Highly protein-bound

154
Q

What lab values monitor warfarin therapeutic concentrations

155
Q

What are the antidotes for warfarin

156
Q

What are 2 treatment for warfarin reversal

A

Recombinant fx 7a

Prothrombin complex concentrate (PCC)

157
Q

Describe the vitamin K compound

A

Fat-soluble vitamin

Requires fat and bile for absorption

158
Q

What are 5 risk factors for vitamin k deficiency

A
  1. Poor dietary intake
  2. Abx therapy killing off gut flora
  3. Malabsorption d/t obstructive biliary tract
  4. Hepatocellular dx
  5. Neonates
159
Q

What organ is Vit K function dependent on

160
Q

How long does vitamin k take to restore concentration of dependent clotting factors

161
Q

Why can’t vitamin K be given IV

A

It can cause life-threatening anaphylaxis

162
Q

What are 4 classes of antiplatelet drugs

A
  1. ADP receptor inhibitors
  2. GpIIb/GpIIIa Receptor antagonists
  3. COX inhibitors
  4. Cox-2 inhibitors
163
Q

What are 4 examples of ADP receptor inhibitors

A

Have -CLO- or -GREL- in the name

  1. CLOpidoGREL
  2. TiCLOpidine
  3. PrasuGREL
  4. TicaGRELor
164
Q

What are 3 examples of GpIIb/IIIa receptor antagonists

A

With an AB or BA (for GpIIB/IIIA

  1. AbciximAB
  2. EptifiBAtide
  3. TirofiBAn
165
Q

What are 2 examples of non-specific COX inhibitors

A

Aspirin

NSAIDs

166
Q

What are 2 examples of COX-2 inhibitors

A

Rofecoxib

Celecoxib

167
Q

What are 4 classes of anticoagulant drugs

A
  1. Heparins
  2. Thrombin inhibitors
  3. Fx 10 inhibitors
  4. Vit K antagonists
168
Q

What are 4 examples of heparin anticoagulants

A 
Unfractionated
1. Heparin
LMWH
2. Enoxaparin
3. Dalteparin
4. Tinzaparin
169
Q

What are 2 examples of thrombin inhibitors

A
  1. Argatroban

2. Bivalirudin

170
Q

What is an example of a Fx 10 inhibitor

A

FondaparinuX

171
Q

How many days before a procedure should ADP receptor inhibitors be stopped

A 
Clopidogrel = 7 days
Ticlopidine = 14 days
Prasugrel = 2-3 days
Ticagrelor = 1-2 days
172
Q

How many days before a procedure should GpIIb/IIIa receptor antagonists be stopped

A 
Abciximab = 3 d
Eptifibatide = 1 d
Tirofiban = 1 d
173
Q

How long before a procedure should thrombin inhibitors be stopped

A 
Argatroban = 4-6 hrs
Bivalirudin = 2-3 hrs
174
Q

How many days before a procedure should warfarin be stopped

175
Q

How do cox inhibitors prevent plt aggregation

A

By blocking COX-1 and stopping conversion of arachidonic acid to PG and ultimately TxA2

176
Q

What is the MOA of aminocaproic acid and TXA

A

Plasminogen activation inhibitor; prevents conversion of plasminogen to plasmin

177
Q

What is the MOA of aprotinin

A

Inhibits plasmin, kallikrein, thrombin, protein C

178
Q

What is the MOA of DDAVP

A

Stimulates factor 8 and vWF factor release

179
Q

What is von Willebrand disease

A

Disorder of plt function

Plt count is normal but do not function properly

180
Q

What are 2 key function of vWF

A
  1. Anchors plt to vessel wall at site of injury (adhesion)

2. Carries inactivated factor 8 in the plasma

181
Q

What are the 3 classifications of von Willebrand disease

A

Type 1 = mild reduction in vWF production
Type 2 = The vWF produced doesn’t work well
Typw 3 = Sever reduction in amount of vWF produced

182
Q

What labs will be altered in a pt with von Willebrand dz

A

PTT = increased
Bleeding time = increased
No changes in PT/INR, Plt count or fibrinogen

183
Q

How does DDAVP aid in procoagulation

A

It stimulates the release of endogenous vWF

Increases Fx 8 activity

184
Q

What coagulopathic disease is DDAVP best suited.

A

Von Willebrand dz type 1

185
Q

DDAVP is a synthetic analog of which hormone

186
Q

Which von Willebrand dz type is DDAVP not appropriate

A

Type 3 dz does not respond to desmopressin

187
Q

Dose for DDAVP

A

0.3 mcg/kg IV

188
Q

Following DDAVP administration, how long before bleeding time improves

189
Q

2 Side effects of desmopressin

A
  1. Vasodilation (esp w/ rapid administration)

2. Hyponatremia (d/t free water retention)

190
Q

What What is the first-line agent for patients with Type 3 von willebrand disease

A

Purified 8-vWF concentrate

The risk of transfusion related issues is decreased

191
Q

What blood products are indicated for treatment of pts with von Willebrand disease

A 
Cryo = has fx 8, 13, fibrinogen, and vWF
FFP = contains all clotting factors
192
Q

What coagulating factors are in cryoprecipitate

A

Fx 8, 13, vWF

Also has fibrinogen

193
Q

What factor is deficient in Hemophilia A

194
Q

What are signs of severe hemophilia A

A

Spontaneous bleeding into joints, muscles, and vital organ

195
Q

Which labs will be altered in pts with hemophilia A and why

A

PTT will be prolonged
B/c fx 8 is part of the intrinsic pathway (PT is not affected)

All other labs are normal

196
Q

What should the pt with hemophilia A receive before surgery

A

Factor 8 concentrate

197
Q

What is the half-life of factor 8 concentrated

198
Q

What other treatment options are available for pts with hemophilia A undergoing surgery

A

FFP
Cryo
DDAVP
TXA (dental procedures)

199
Q

What should always be available for pts with hemophilia A undergoing surgery

A

Type and crossmatch

200
Q

What is hemophilia B

A

Factor 9 deficiency

201
Q

What treatment can be given prior to surgery in pts with hemophilia B

A

Factor 9-prothrombin complex concentrate

202
Q

What is the dose for recombinant factor 7

A

90-120 mcg/kg

203
Q

In which pts can recombinant factor 7 be useful

A

Hemophilia A or B pts that develop inhibitor that prevent exogenous Fx 8 or 9 from achieving therapeutic goals

204
Q

What are the risks of giving recombinant factor 7 in hemophilia pts

A

It can increase the risk of arterial thrombosis (MI or embolic stroke) or venous thrombosis

205
Q

What is DIC

A

disseminated intravascular coagulation

It is characterized by simultaneous hemorrhage and systemic thrombosis

206
Q

What become deficient with DIC and why

A

Plt, fibrinogen, and clotting factors

Because they are consumed from being used to stop bleeding while forming microvascular thrombi

207
Q

What labs are altered in DIC

A 
PT/PTT = increased
D-Dimer = increased
Plt = decreased
Fibrinogen =  decreased
208
Q

What causes tissue hypoxia and acidosis in DIC

A

Generalized thrombin formation that creates microvascular clots impairing tissue perfusion. Leads to organ failure

209
Q

Why is hemorrhage a problem in DIC

A

Due to widespread fibrin deposition, fibrinogen, coag factors, and plts are consumed. There is nothing left for hemostasis where it is needed

210
Q

Are fibrinolytics part of DIC

A

Yes, Release of tPA and urokinase-type plasminogen activator occurs

211
Q

What are 7 signs of DIC

A
  1. Ecchymosis
  2. Petechiae
  3. Mucosal bleeding
  4. Bleeding at IV puncture sites
  5. Prolonged PT/PTT
  6. Increased D Dimer
  7. Decreased fibrinogen and AT
212
Q

What 3 conditions are associated with high risk for developing DIC

A
  1. Sepsis (gram-neg bacilli)
  2. Obstetric complications (pre-E, placental abruption, AFE)
  3. Malignancy (adenocarcinoma, leukemia, lymphoma)
213
Q

What is affected by AT deficiency

A

The ability to inactivate Fx 9, 10, 11, and 12 leading to thrombin (2a) inhibition

Heparin responsiveness

214
Q

What are pts with AT deficiency at risk for

215
Q

Treatment for AT deficiency

A

AT concentrate

FFP

216
Q

What is the etiology of heparin-induced thrombocytopenia

A

The body initiates an immune response against heparin after it binds to plt factor 4
IgG antibodies activate platelets resulting in uncontrolled clot formation

217
Q

Why is the plt count low during HIT

A

Because the plt have been activated by IgG antibodies and used to form widespread clots

218
Q

What is the difference in pathology between HIT type 1 and 2

A

Type 1 = heparin induced plt aggregation

Type 2 = Antiplatelet antibody IgG attack factor 4 immune complex causing plt aggregation

219
Q

What is the precipitating event of HIT type 1 vs type 2

A

Type 1 = large heparin doses

Type 2 = any heparin dose

220
Q

What is a typical plt count in HIT type 1 vs type 2

A

Type 1 < 100,000

Type 2 < 50,000

221
Q

What is the onset of HIT type 1 vs type 2

A

Type 1 = 1-4 days post heparin

Type 2 = 5-14 days post heparin

222
Q

What is the coagulation status in HIT type 1 vs type 2

A

Type 1 = minimal

Type 2 = hypercoagulable

223
Q

What is the treatment for HIT type 2

A

Direct thrombin inhibitors:
Bivalirudin
Hirudin
Argatroban

224
Q

What is the function of protein C

A

Anticoagulant effect by inhibiting Fx 5a and 8a

225
Q

What is protein S

A

a co-factor of protein C

226
Q

What is the result of protein C or S deficiency

A

Hypercoagulable state

Increased risk of thrombosis

227
Q

What is the treatment of protein C or S deficiency

A

Initial thromboembolic event is treated with heparin, then pt transitioned to warfarin

228
Q

What is Factor 5 Leiden mutation

A

Resistance to anticoagulant effect of protein C

229
Q

What are 4 thrombotic disorders

A
  1. AT deficiency
  2. HIT
  3. Protein C or S deficiency
  4. Factor 5 Leiden mutation
230
Q

3 ways the RBC function is affected by sickle cell disease

A
  1. Deoxygenation of hgbS leads to sickling
  2. Sickling causes RBCs to clump and cause obstruction in microvasculature, impairing tissue perfusion
  3. Sickle cells are more prone to hemolysis and removal by spleen (shorter life-span)
231
Q

What does anesthetic management of the pt with sickle cell disease focus on

A

Preventing the following:

  1. Pain
  2. Hypothermia
  3. Hypoxemia
  4. Acidosis
  5. Dehydration
232
Q

How is a sickle cell vaso-occlusive crisis treated

A

Analgesia

IV hydration

233
Q

What is the result of a vaso-occlusive crisis

A

Impaired tissue perfusion

Ischemic injury

234
Q

What causes acute chest syndrome in pts with sickle cell disease

A 
Thrombosis
Embolism
Infection
Hypoventilation
Narcotics
Splinting
Pain
235
Q

Diagnosis parameters for acute chest syndrome in sickle cell disease

A

CXR with new lung infiltrates

One of the following symptoms: chest pain, dyspnea, cough, wheezing

236
Q

When is acute chest syndrome most likely to occur

A

in the postoperative period

237
Q

What is a sequestration crisis

A

When the spleen removes RBCs from circulation at a faster rate than the bone marrow produces them leading to anemia and hemodynamic instability

238
Q

What can cause an aplastic crisis and how is it manifested

A

Causes = viral infection (parvovirus B19)

Manifestation = Bone marrow suppression can cause anemia

APEX-Fluids and Blood (3 decks)

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