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APEX > Unit 9 - Coagulation > Flashcards

Unit 9 - Coagulation Flashcards

1
Q

tunica media is thicker in arteries or veins?

A

arteries

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2
Q

thinnest vascular layer in veins

A

tunica externa

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3
Q

how does the body attempt to prevent hemorrhage with vascular injury?

A
  1. vascular spasm
  2. formation of platelet plug
  3. coagulation and fibrin formation
  4. fibrinolysis when clot no longer needed

4 steps of homeostasis

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4
Q

primary step of homeostasis

A

formation of platelet plug

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5
Q

function of von willebrand factor

A

platelet adhesion

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6
Q

function of collagen

A

tensile strength

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7
Q

function of fibronectin

A

cell adhesion

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8
Q

function of thrombomodulin

A

regulates naturally occuring anticoagulants

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9
Q

function of protein C

A

degrades factor 5a & 8a

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10
Q

degrades factor 5a & 8a

A

protein C

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11
Q

cofactor for protein C

A

protein S

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12
Q

degrades factors 9a, 10a, 11a, 12a

A

antithrombin

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13
Q

function of antithrombin

A

degrades factors 9a, 10a, 11a, 12a

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14
Q

precursor to plasmin

A

plasminogen

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15
Q

activates plasmin

A

tPA
urokinase

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16
Q

inactivates tPA & urokinase

A

alpha-antiplasmin

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17
Q

inhibits plasmin

A

plasmin activator inhibitor

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18
Q

vasoactive mediators responsible for vascular smooth muscle constriction

A

thromboxane A2
ADP
serotonin

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19
Q

vasoactive mediators responsible for vascular smooth muscle relaxation

A

nitric oxide
prostacyclin

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20
Q

produces platelets in bone marrow

A

megakaryocytes

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21
Q

where are platelets produced

A

bone marrow

by megakaryocytes

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22
Q

normal platelet value

A

150-300k

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23
Q

lifespan of a platelet

A

8-12 days

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24
Q

how are platelets cleared

A

by macrophages in reticuloendothelium & spleen

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25
Q

what organ can sequester up to 1/3 of all circulating platelets for later use

A

spleen

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26
Q

why are plts pushed towards vessel wall close to site of action

A

smaller size

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27
Q

where do glycoproteins adhere

A

injured endothelium, collagen, and fibrinogen

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28
Q

2 components of platelet external membrane

A

glycoproteins
phospholipids

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29
Q

7 components inside the plts

A
  1. actin/myosin
  2. thrombosthenin
  3. ADP
  4. calcium
  5. fibrin-stabilizing factor
  6. serotonin
  7. growth factor
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30
Q

function of actin & myosin inside platelet

A

help contract to form plt plug

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31
Q

function of thrombosthenin inside the platelet

A

help with platelet activation & aggregation

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32
Q

function of ADP inside platelet

A

plt activation & aggregation

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33
Q

function of calcium inside platelet

A

multiple functions in coagulation cascade (factor 4)

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34
Q

function of serotonin inside plts

A

activates nearby plts

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35
Q

function of growth factor inside platelet

A

helps repair damaged vessel walls

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36
Q

what keeps blood as a liquid when there’s no injury

A
  1. coagulation proteins circulate in inactive form
  2. glycocalyx repels clotting factors
  3. smooth endothelium prevents activation of plts/coagulation
  4. activated factors removed by brisk blood flow/circulating anticoagulants
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37
Q

how does the endothelium inhibit plt function in the absence of vascular injury

A

secretes prostaglandin 12 & nitric oxide

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38
Q

substrate for prostaglandin synthesis

A

phospholipids

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39
Q

what produces thromboxane A2

A

phospholipids

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40
Q

what does the GpIIb complex do

A
  • attaches activated platelet to vWF
  • links platelets together to form plug
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41
Q

how does nitric oxide inhibit platelet function

A

inhibits thromboxane A2 receptor

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42
Q

how does prostaglandin 12 help inhibit plt function

A
  • inhibits vWF adherence
  • thromboxane A2 activation
  • release of storage granules
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43
Q

common sources of endothelial injury

A
  • surgery
  • trauma
  • plaque dislodgment
  • spontaneous micro-injury (occur daily)
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44
Q

what part of the vessel contracts immediately following injury

A

tunica media

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45
Q

tunica media contraction with injury is the result of what 3 functions

A
  1. SNS reflexes
  2. myogenic response
  3. release of vasoactive substances
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46
Q

2 functions of vascular spasm

A
  1. reduces blood loss
  2. helps procoagulants remain in affected area
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47
Q

3 steps of primary homeostasis

A
  1. adhesion
  2. activation
  3. aggregation
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48
Q

how long does the process to form a plt plug take

A

about 5 min

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49
Q

what happens in step 1 of platelet plug formation

A

adhesion
plts immediately adhere to exposed collagen with help of vWF

endothelial injury exposes collagen

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50
Q

how do plts adhere to collagen in step 1 of primary homeostasis

A

via Gp Ia/IIa and Gp VI receptors

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51
Q

how long does it take for platelets to adhere to collagen after vascular injury

A

within seconds

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52
Q

where is von Willebrand factor synthesized and released from

A

endothelium

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53
Q

where does vWF bind to platelet to bind to subendothelium

A

to GpIb receptor

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54
Q

step 2 of primary homeostasis

(formation of plt plug)

A

plts contract and release series of compounds that attract other plts to site

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55
Q

how are platelets activated in step 2 of primary homeostasis

A

exposed collagen at site of injury activates plts

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56
Q

2 substances released by activated platelets

A

ADP
thromboxane A2

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57
Q

responsible for adhering platelet to damaged vessel

A

von willebrand factor

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58
Q

what do activated plts release in step 2 of primary homeostasis

A

contents of alpha granules
* fibrinogen
* fibronectin
* vWF
* platelet factor 4
* platelet growth factor

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59
Q

2 glycoproteins expressed on surface of activated platelets

A

GpIIb
GpIIIa

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60
Q

links activated platelets together to form platelet plug

A

GpIIb/IIIa receptor complex

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61
Q

step 3 of primary homeostasis

A

aggregation
plt plug forms

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62
Q

required to configure GpIIb and GpIIIa

A

Thromboxane A2
ADP

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63
Q

what is needed to mesh wound in micro-injuries

A

a platelet plug is all that’s needed
(activation of coagulation cascade not needede)

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64
Q

primary purpose of coagulation cascade

A

form fibrin

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65
Q

in the classic coagulation model, when is the extrinsic pathway activated

A

when coagulation initiated outside intravascular space

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66
Q

in the classic coagulation model, when is the intrinsic pathway activated

A

when coagulation initiated inside intravascular space

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67
Q

how is coagulation activated in the cell based model

A

by extrinsic pathway as injured endothelium releases tissue factor 3

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68
Q

endpoint of classic model of coagulation

A

2 distinct pathways
each arrives st final common pathway

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69
Q

function of intrinsic pathway in cell based model

A

amplifies thrombin generating effect of extrinsic pathway

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70
Q

factors in coagulation cascade

A

1 fibrinogen
2 prothrombin
3 tissue factor
4 calcium ions
5 labile factor
7 stable factor
8 antihemophilic factor
9 christmas factor
10 stuart-prower factor
11 plasma thromboplastin antecedant
12 hageman factor
13 fibrin stabilizing factor

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

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70
Q

factors in coagulation cascade

A

1 fibrinogen
2 prothrombin
3 tissue factor
4 calcium ions
5 labile factor
7 stable factor
8 antihemophilic factor
9 christmas factor
10 stuart-prower factor
11 plasma thromboplastin antecedant
12 hageman factor
13 fibrin stabilizing factor

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

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71
Q

where are factors in coagulation cascade synthesized

A

liver
except tissue factor (vascular wall) & calcium (diet)

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72
Q

lab test for intrinsic pathway

A

PTT, ACT

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73
Q

lab tests for extrinsic pathway

A

PT/INR

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74
Q

vitamin-k dependent clotting factors

A

2, 7, 9, 10

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75
Q

1st coagulation factor activated in extrinsic pathway

A

tissue factor

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76
Q

activates extrinsic pathway

A

tissue factor

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77
Q

factors of extrinsic pathway

A

3 & 7

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78
Q

first factor to become deficient in liver failure, vitamin K deficiency, and pts on warfarin

A

factor 7

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79
Q

coagulation factor with the shortest half life

A

factor 7
(4-6 hours)

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80
Q

how much time does extrinsic pathway take

A

~15 seconds

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81
Q

collective coagulation factors that lead to thrombin activation (2a)

A

prothrombin activator
aka prothrombinase

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82
Q

how is factor 10 activated in extrinsic pathway

A
  • tissue trauma activates tissue factor
  • tissue factor activates factor 7
  • factor 7 activates factor 10 in presence of 4 calcium
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83
Q

positive feedback mechanism that accelerates continued production of prothrombin activator in extrinsic pathway

A

factor 5

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84
Q

factors specific to classical intrinsic pathway

A

8, 9, 11, 12

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85
Q

steps of extrinsic pathway

A
  1. tissue factor release
  2. factor 10 activation
  3. prothrombin activator
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86
Q

steps of intrinsic pathway

A
  1. blood trauma exposure to collagen
  2. factor 11 activation
  3. factor 9 activation
  4. factor 10 activation
  5. prothrombin activator
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87
Q

time for intrinsic pathway to form a clot

A

6 minutes

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88
Q

what happens in first step of intrinsic pathway

A

blood trauma exposure to collagen = factor 12 activation

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89
Q

how is factor 11 activated in intrinsic pathway

A

factor 12a

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90
Q

what is required for factor 12a to activate factor 11 in intrinsic pathway

A

HMW kininogen

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91
Q

what acceperates factor 12a activation of factor 11

A

prekallikrein

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92
Q

what activates factor 9 in intrinsic pathway

A

factor 11

93
Q

how is factor 10 activated in intrinsic pathway

A

by factor 9a & 8

94
Q

what factor is missing in hemophilia A

A

8

95
Q

how is thrombin (factor 2a) activated in intrinsic pathway

A

prothrombin activator & tissue phospholipids

identical to last step of extrinsic pathway

96
Q

how is thrombin (factor 2a) activated in intrinsic pathway

A

prothrombin activator & tissue phospholipids

identical to last step of extrinsic pathway

97
Q

factors involved in final common pathway

A

5, 10, 1, 2, 13

“The final common pathway can be purchased at the five (5) and dime (5) for 1 or 2 dollars on the 13th of the month”

97
Q

factors involved in final common pathway

A

5, 10, 1, 2, 13

“The final common pathway can be purchased at the five (5) and dime (5) for 1 or 2 dollars on the 13th of the month”

98
Q

factors involved in final common pathway

A

5, 10, 1, 2, 13

“The final common pathway can be purchased at the five (5) and dime (5) for 1 or 2 dollars on the 13th of the month”

99
Q

primary goals of intrinsic and extrsinic pathway in final common pathway

A

produce prothrombin activator

100
Q

when does final common pathway begin

A

when prothrombinase (complex of 10z + 5a + 4) converts prothrombin (2) to thrombin (2a)

101
Q

proteolytic enzyme that changes fibrinogen to fibrinogen monomer

A

thrombin (2a)

102
Q

when is fibrin incorporated into platelet plug in final common pathway

A

after platelets aggregate

103
Q

facilitates cross-linkage of fibin fibers to complete clot in final common pathway

A

factor 13a
activated fibrin-stabilizing factor

104
Q

4 mechanisms that counterbalance clot formation

A
  1. vasodilation/washout of ADP & TXA2
  2. anththrombin actions
  3. tissue factor pathway inhibitor
  4. protein C & S
105
Q

how does antithrombin counterbalance clot formation

A

inactivates thrombin (2a), 9a, 10a, 11a, & 12a

106
Q

how do proteins C & S counterbalance clot formation

A

inhibit factors 5a and 8a

107
Q

where is plasminogen synthesized

A

liver

108
Q

function of plasminogen

A

proenzyme incorporated into clot as it’s being formed (dormant until activated)

109
Q

what is plasmin

A

proteolytic enzyme that degrades fibrin into fibrin degradation products

110
Q

2 enzymes that convert plasminogen to plasmin

A

tPA
urokinase

111
Q

major mechanism of plasmin activation

A

injured tissue releases tissue plasminogen activator (tPA) over a period of days

112
Q

minor mechanism of plasmin formation

A

urokinase produced by kidneys and released into circulation

113
Q

where is urokinase produced

A

kidneys

114
Q

how are plasmin activators used therapeutically

A

to dissolve thrombi and restore blood flow

115
Q

inhibits conversion of plasminogen to plasmin

A

tPA inhibitor (tPAI)

116
Q

inhibits action of plasmin on fibrin

A

alpha-2 antiplasmin

117
Q

3 phases of contemporary cell-based coagulation cascade

A
  1. initiation
  2. amplification
  3. propagation
118
Q

when does the initiation phase of the contemporary coagulation cascade begin

A

when tissue factor is expressed

119
Q

what factors begin the initiation phase of contemporary coagulation cascade

A

3 & 7

120
Q

thrombin levels during initiation phase of contemporary coagulation cascade

A

remain low bc tissue factor pathway inhibitor limits amount of tissue factor released

121
Q

why isn’t fibrin activated in the initiation phase of the contemporary coagulation cascade

A

quantity of thrombin produced is insufficient to activate thrombin

122
Q

lays groundworn for large-scale thrombin production in amplification phase of contemporary coagulation cascade

A

platelets and cofactors

123
Q

how does the small amount of thrombin produced on TF-bearing cells amplify the coagulation response
(contemporary coagulation cascade)

A

by activating platelets, factor 5, and factor 11

124
Q

what happens in the propagation phase of the contemporary coagulation cascade

A

Large quantities of thrombin are produced on the surfaces of platelets

125
Q

when does propagation phase begin (contemporary coagulation cascade)

A

factor 10 is activated by factors 4 (Ca+2), 8, and 9 on the surface of the platelet

126
Q

which phase of contemporary coagulation cascade is a positive feedback mechanism

A

propagation phase

produces enough thrombin to activate fibrin

127
Q

which phase of contemprary coagulation cascade is a positive feedback mechanism

A

propagation phase

produces enough thrombin to activate fibrin

128
Q

what coagulation pathways does aPTT assess

A

intrinsic
final common

129
Q

best predictor of bleeding during surgery

A

history & physical

130
Q

what does aPTT measure

A

time it takes to form a clot using phospholipid, calcium, and an activator

131
Q

Monitors therapeutic response to unfractionated heparin (not LMWH)

A

aPTT

132
Q

factors included in intrinsic pathway

A

12
11
9
8

133
Q

coagulation pathway inhibited by heparin

A

intrinsic

134
Q

what is the role of thrombin

A

converts fibrinogen to fibrogen monomer

135
Q

what must be present to convert fibrogen monomer to fibrin fibers

A

calcium (factor 4)

136
Q

converts fibrin to fibrin degredation products

A

plasmin

137
Q

measures fibrin degradation products

A

D-dimer

138
Q

inhibits conversion of plasminogen to plasmin

A

tPA

139
Q

normal aPTT value

A

25-32 seconds

140
Q

why is normal aPTT longer than normal PT

A

the intrinsic pathway is slower than extrinsic

141
Q

at what point will a change in aPTT occur

A

factors must be reduced by > 30%

142
Q

what pathways does PT assess

A

extrinsic & final common

143
Q

what 2 enzyme inhibitors turn off the fibrinolytic process

A
  1. tPAI
  2. alpha 2 antiplasmin
144
Q

how are plasmin activators used therapeutically

A

dissolve thrombi to restore flow

145
Q

what does PT measure

A

time it takes to form a clot using tissue factor and calcium

146
Q

which lab test monitors therapeutic response to warfarin

A

PT

147
Q

normal PT

A

12-14 seconds

148
Q

when will a decrease in PT be seen

A

Factors must be reduced by > 30% before a change in PT is observed

149
Q

calculation that standardizes PT results

A

INR

150
Q

what is INR based on

A

ratio between patient’s PT and the standard mean PT

151
Q

normal INR in healthy pts

A

~1

152
Q

target INR for pts on warfarin

A

2-3x control

153
Q

lab that guides heparin dosing

A

ACT

154
Q

normal ACT

A

90-120 seconds

Should be > 400 seconds before going on CPB

155
Q

normal ACT

A

90-120 seconds

Should be > 400 seconds before going on CPB

156
Q

when is ACT measured

A

before heparin admin, 3 minutes after it’s given, and every 30 min thereafter

157
Q

what lab tends to be more accurate when large doses of heparin are given

A

ACT > PTT

158
Q

factors that affect ACT

A
  • hypothermia
  • thrombocytopenia
  • deficiency of fibrinogen
  • deficiency of factor 7
  • deficiency of factor 12
159
Q

plt count that indicates inc surgical bleeding risk

A

< 50,000

160
Q

plt count that indicates inc surgical bleeding risk

A

< 50,000

161
Q

plt count that indicates increased spontaneous bleeding risk

A

<20,000

162
Q

plt count that indicates increased spontaneous bleeding risk

A

<20,000

163
Q

lab test that monitors platelet function

A

bleeding time

164
Q

normal bleeding time value

A

2-10 minutes

165
Q

what drugs prolong bleeding time

A

aspirin
NSAIDs

166
Q

what does D-dimer monitor for

A

fibrinolysis (fibrin degradation products)

167
Q

what does increased d-dimer indicate

A

fibrinolysis
if increased, likely a thrombus present

168
Q

differential with increased D-dimer

A

DVT
PE
DIC

169
Q

Provides a “real time” visual representation of disorders of coagulation & fibrinolysis

A

TEG

170
Q

TEG: R time

A

time to begin forming clot

171
Q

normal R time (TEG)

A

6-8 minutes

172
Q

treatment for prolonged R time
(TEG)

A

FFP

173
Q

TEG: K time

A

time until clot has achieved fixed strength

174
Q

normal value of K time (TEG)

A

3-7 minutes

175
Q

treatment for prolonged K time (TEG)

A

cryo

176
Q

what is the alpha angle in a TEG result

A

speed of fibrin accumulation

177
Q

treatment of increased alpha angle (TEG)

A

cryo

178
Q

normal alpha angle (TEG)

A

50-60 degrees

179
Q

what is maximum amplitude of TEG

A

highest verticle amplitude

measures clot strength

180
Q

what is A60 on TEG

A

height of verticle amplitude 60 min after max amplitude

181
Q

normal A60 value (TEG)

A

MA - 5

182
Q

what does an increased A60 in TEG indicate

A

excess fibrinolysis

183
Q

treatment of increased A60

A

TXA
Amicar

184
Q

produces endogenous heparin

A

basophils, mast cells, and the liver

185
Q

what is exogenous heparin derived from

A

bovine lung and pig GI mucosa

186
Q

naturally occurring anticoagulant that circulates in plasma

A

antithrombin

187
Q

pathways inhibited by heparin

A

intrinsic
final common

188
Q

MOA of heparin

A
  • binds to AT and greatly accelerates its anticoagulant ability (1000-fold)
  • heparin-AT complex neutralizes thrombin & activated factors 9, 10, 11, and 12

also inhibits platelet function

189
Q

MOA of heparin

A
  • binds to AT and greatly accelerates its anticoagulant ability (1000-fold)
  • heparin-AT complex neutralizes thrombin & activated factors 9, 10, 11, and 12

also inhibits platelet function

190
Q

MOA of heparin

A
  • binds to AT and greatly accelerates its anticoagulant ability (1000-fold)
  • heparin-AT complex neutralizes thrombin & activated factors 9, 10, 11, and 12

also inhibits platelet function

191
Q

what should be considered if heparin fails to adequately anticoagulate

A

AT deficiency

192
Q

Vd of heparin

A

small

193
Q

how is heparin metabolized

A

heparinase

194
Q

2 pathways for heparin elimination

A
  1. degradation by macrophages
  2. renal excretion
195
Q

is heparin safe in pregnancy

A

yes - does not cross placenta

196
Q

1 unit heparin =

A

the volume of heparin-containing solution that prevents 1 mL of citrated sheep blood from clotting for one hour following the addition of 0.2 mL of 1:100 CaCI

197
Q

heparin dosing. for cardiac surgery

A

300-400 units/kg IV

198
Q

heparin dosing for VTE prophylaxis

A

5,000 U SQ BID or TID

199
Q

heparin dosing for active VTE

A

5,000 U IV then infusion of ~ 1,250 U/hr to maintain aPTT 1.5 - 2.5x normal

200
Q

heparin dosing for unstable angina & MI

A

5,000 U IV then infusion of 1,000 U/hr

201
Q

aPTT that indicates therapeutic heparinization

A

1.5-2.5x normal
(normal = 25-35 sec)

202
Q

Side effects of heparin

A
  • hemorrhage
  • heparin-induced thrombocytopenia (HIT)
  • allergic reaction
  • hypotension
  • decreased antithrombin concentration
203
Q

heparin contraindications

A

NSGY
HIT
regional anesthesia

204
Q

MOA of protamine

A

highly alkaline, strong positive charge + negative charge of heparin = neutralization reaction that stops heparin’s anticoagulant

205
Q

dosing protamine

A

1 mg protamine for every 100 U heparin predicted to be in circulation

206
Q

how is the heparin-protamine complex cleared

A

Reticuloendothelial system

207
Q

function of protamine when given alone

A

anticoagulant

208
Q

3 side effects of protamine

A
  1. hypotension
  2. pulmonary HTN
  3. allergic reaction
209
Q

what causes hypotension with protamine

A

histamine release

give over > 5 min

210
Q

what causes pulmonary HTN with protamine

A

thromboxane A2 and serotonin release

211
Q

factors that increase risk of allergic reaction to protamine

A
  • sensitization to NPH insulin
  • fish allergy
  • vasectomy
  • multiple allergies
212
Q

MOA of warfarin

A

Inhibits the enzyme vitamin K epoxide reductase complex 1 (VKOR c1)

213
Q

factors indirectly inhibited by warfarin

A
214
Q

responsible for converting inactive vitamin K to active vitamin K

A

vitamin K epoxide reductase complex 1 (VKOR c1)

inhibited by warfarin

215
Q

factors indirectly blocked by warfarin

A

vitamin-K dependent (2, 7, 9, 10)
proteins c and s

216
Q

protein binding of warfarin

A

highly protein bound

217
Q

how long required to achieve therapeutic concentration of warfarin

A

36-72 hours

218
Q

warfarin antidote

A

Vitamin K and FFP

219
Q

how to reverse warfarin for emergent or high-risk procedures

A

1-2 units FFP, recombinant factor 7a, or prothrombin complex concentrate

high risk = NSGY procedures

220
Q

how to reverse warfarin for non-emergent minor surgical procedures

A

10-20 mg vitamin K

221
Q

how is plasminogen converted to plasmin

A

by tPA

222
Q

what is required for absorption of vitamin K

A

presence of fat and bile for absorption

223
Q

risk factors for vitamin K deficiency

A
  1. poor dietary intake
  2. antibiotics
  3. malabsorption d/t obstructive biliary tract disease
  4. Hepatocellular disease
  5. Neonates
224
Q

what is phyntonadione

A

exogenously administered vitamin K

225
Q

required for exogenous vitamin K admin

A

a functional liver

226
Q

how long does it take for exogenous vitamin K to restore concentration of vitamin K-dependent clotting factors in blood

A

4-8 hours

227
Q

phytonadione dose

A

10-20 mg IV, IM, PO

228
Q

risk assoc with IV phytonadione

A

life threatening anaphylaxis
avoid IV or give max. 1mg/min

APEX (54 decks)

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