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Coagulation > Hemostasis 1.c.7 > Flashcards

Hemostasis 1.c.7 Flashcards

1
Q

what is the definition of hemostasis

A

keeping the blood within the fluidic state within the confines of the vascular system

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2
Q

what is in the plasma layer

A

water
proteins
clotting factors
gamma globulins

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3
Q

what is in the Buffy coat

A

WBC

platelets

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4
Q

what is in the RBC layer

A

O2 carrying capacity

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5
Q

within the vascular system, there can be endothelial damage. What is the effects of endothelial damage?

A
  • activation of platelets
  • activation of plasma coagulation
  • release of inhibitors
  • initiation of fibrinolysis
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6
Q

what is the name of the place where the two platelets come together

A

the IIB3AC receptor site

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7
Q

Platelets is a ____ shape and is approx _____ microns in diameter

A

discoid shape and about 2-4 microns in diameter

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8
Q

Approximately 1/3 of platelets is sequestered in the

A

spleen

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9
Q

what do platelets act as

A

early responders to vascular damage

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10
Q

what is the “mothership” of platelet formation?

A

megakaryocytes, which is a large precursor cell with multiple nuclei

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11
Q

where are megakaryocytes normally present

A

only in bone marrow

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12
Q

what is the large precursor cell that has multiple nuclei that creates platelet?

A

megakaryocytes

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13
Q

how do platelets come from megakaryocytes

A
  • platelets bud from cell cytoplasm

- squeeze through the marrow sinusoids into peripheral circulation

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14
Q

all coagulation factors are synthesized by the liver except for

A

portion of Factor VIII (endothelium and megakaryocytes)

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15
Q

Roman numeral designation except for

A

high molecular weight kininogen (HMWK)
&
pre-kalekron (PK)

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16
Q

Coagulation factors function as

A
  • cofactors (V and VIII)
  • enzymes (active form)
  • substrate (fibrinogen or factor I)
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17
Q

end result of coagulation factors interaction leads to

A

fibrin formation = solid clot

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18
Q

what is the “fast pathway of clotting”

A

the extrinsic pathway

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19
Q

what is an example of when the extrinsic “fast pathway” is activated

A
  • make an incision and shoving things up there to find a vein
  • incision in chest
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20
Q

how does temperature effect coagulation

A

heat it up = make it go faster

cool it down = flow it down

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21
Q

“long pathway of clotting” occurs when

A

due to bypass or foreign surfaces

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22
Q

___ ____ _____ is what leads to coagulation

A

free floating thrombin

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23
Q

what is the 1st largest protein in the body

A

albumin

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24
Q

what is the 2nd largest protein in the body

A

fibrinogen

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25
Q

what is the 3rd largest protein in the body

A

gamma globulins

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26
Q

Free floating thrombin regulates what coagulation reactions

A

factors V and VIII

factors XI

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27
Q

what turns fibrinogen into fibrin

A

thrombin

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28
Q

when you hear John Hageman, what should come to mind?

A

factor XII

contact/activating factor

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29
Q

what is the physiological activator of normal hemostasis?

A
  • Tissue factor-FVIIa complex

- the fast pathway

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30
Q

in normal hemostasis and at the molecular level, where does the interaction of coagulation factors take place?

A

on the surface of activated platelets

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31
Q

what is the definition of fibrinogen

A

break up of a clot

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32
Q

what’s a D-dimer?

A

when you got a clot, plasminogen breaks it up into little split products

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33
Q

If you have D-dimers, what does that mean

A

you have activated plasminogen which you NEVER WANT TO HAVE ON BYPASS

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34
Q

clot formation come from

A

coagulation elements

high suctioning

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35
Q

protein C/S in presence of thrombin forms

A

activated protein C (APC)

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36
Q

what does APC do

A

inactivate factors Va and VIIIa

inhibits activation of factors X and II

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37
Q

what is required to synthesis for liver?

A

vitamin K required

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38
Q

____ _ is a major physiological inhibitor of coagulation

A

protein C

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39
Q

____ _ is a cofactor for Protein C

A

protein S

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40
Q

how often is protein C/S deficiency seen in the general population?

A

2-3%

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41
Q

what are some clinical manifestations of protein C/S deficiency?

A
  • DVT
  • PE
  • homozygous protein C deficiency-neonatal purpura fulminans
  • warfarin-induced skin necrosis following warfarin initiation in Protein C deficiency
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42
Q

what does ATIII inhibit?

A

thrombin, 9, 10, 11, clotting factors

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43
Q

where do you get heparin in the body

A

mast cells in lung

vonkufer in the liver

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44
Q

what is AntithrombinIII synthesized by

A

liver and endothelial cells

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45
Q

what can increase the activity of antithrombinIII by several thousand fold?

A

heparin

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46
Q

when does ATIII deficiency appear and what is it an increased risk for

A

onset usually appears in young adulthood

-increased risk of venous thrombosis

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47
Q

acquired ATIII deficiency can be seen if you have these characteristics….

A 
acute thrombosis 
DIC (disseminated intravascular coagulation) 
liver disease 
nephrotic syndrome
oral contraceptive use
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48
Q

where does heparin work?

A

where AT3 is

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49
Q

where does AT3 work?

A 
thrombin (IIa) 
Xa
IXa 
XIa 
XIIa
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50
Q

why do we not want to activate plasminogen

A

can lead to bradykinin

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51
Q

what is kinin mechanism involved in

A

inflammatory response and wound healing

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52
Q

what are some things bradykinin does? (6)

A
  • increase vascular permeability
  • vasodilation
  • smooth muscle contraction
  • inflammation, phagocytosis
  • pain
  • tissue repair
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53
Q

what does complement destroy?

A

collateral damage

destroys good and bad tissue in its effort to destroy whatever made it mad

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54
Q

why do you zbuff

A

removing complement components

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55
Q

what can activate complement? (4)

A
  • foreign substances such as bacteria and viruses
  • components of the cardiopulmonary bypass system
  • materials used in the collection and processing of autologous blood
  • damage red blood cells: blood recovered from the operative site for auto transfusion
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56
Q

activation of complement results in

A
  • macromolecular attack complex

- cell destruction and inflammatory response

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57
Q

classical pathway fro complement

A 
antigen -Ig complex 
to 
formation of C3 convertase 
to 
MAC (membrane attack complex)
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58
Q

alternative pathway for complement

A 
pathogen surface antigen 
to 
formation of C3 convertase 
to 
peptides to increase inflammation and increase chemotasix
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59
Q

Together with activating plasminogen, bradykinin and all that leads toooooo

A

systemic inflammatory response

60
Q

without fixing a systemic inflammatory response, can lead to

A

inhibit organ perfusion and multi system failure

61
Q

when does SIRS occur

A
  • overhwhelming sepsis
  • severe trauma
  • burns
  • CPB
62
Q

SIRS results in a whole body or systemic inflammatory response with disorders of

A

microcirculation and organ perfusion

63
Q

SIRS leads to activation of cellular and humoral pathways such as (3)

A
  • plasma coagulation/fibrinolysis
  • complement activation and kinin generation
  • activation of platelets and leukocytes
64
Q

cooling has a big effect on anticoagulation because

A

it is an enzymatic process and if you cool it down, you slow it down

65
Q

Contact activation occurs throughout all of CPB because

A

all foreign surfaces when inserting cannula and running blood through circuit

66
Q

kinin generation activates

A

complement and antiforeign response

67
Q

CPB effects on hemostasis (9)

A
  • hemodilution
  • hypothermia
  • factor VII/tissue factor activation
  • contact activation (XII)
  • kinin generation
  • activation of complement and systemic inflammatory response
  • shear stress (platelet activation)
  • fibrinolysis
  • anticoagulation/reversal
68
Q

do we care about factor XII

A

YES

69
Q

factor 12 activates factors

A

5, 8, 11

70
Q

goals for anticoagulation

A
  • prevent thrombus formation
  • preserve patient’s hemostatic elements
  • prevents SIR (systemic inflammatory response)
71
Q

what are some anticoagulant/antithrombotic agents (5)

A 
heparin
direct thrombin inhibitors 
oral anticoagulants 
platelet inhibitors
thrombolytics
72
Q

characteristics of unfractionated heparin (UHF(

A
  • heterogeneous substance (get it in different places in nature)
  • mw: 5,000 to 30,000
  • source: pig guts
  • half life: 45-60 minutes
  • bi phasic elimination
73
Q

heparin + _____ is required for anticoagulant action

A

antithrombin III

74
Q

what does UFH inhibit?

A

free thrombin and other activated coagulation proteins

75
Q

after 7-10 minutes, how much of heparin has been eliminated?

A

1/3 of heparin is not available for AT3

76
Q

for unfractionated heparin, what is the mechanism of action?

A
  • enhances the inhibition by AT3 of thrombin(IIa) and other serine proteases
  • heparin finds an ATIII and hits it and makes conformational changes on the receptor site on molecule so it can now bind and hold onto thrombin
77
Q

how do you neutralize heparin?

A

by protamine sulfate

  • protamine is administered, grabs the heparin complex
  • AT3 can no longer make the conformational changes it needs to hold to thrombin
78
Q

uses of UFH (9)

A
  • cardiac surgery
  • ECMO
  • VADS
  • cardiac Cath lab
  • IR
  • Dialysis
  • Therapeutic
  • Prophylactic
  • prevent arterial and venous lines from clotting
79
Q

what is important for anticoagulation regarding heparin?

A

provide sufficient drug to achieve anticoagulant and antithrombotic effect
-base on: size, sex, adult vs peds

80
Q

what are the clinical laboratory test that can be done to monitor UFH?

A
  • activated partial thromboplastin time (APTT): functional/qualitative, assess inhibition o plasma coagulation by heparin
  • anti-Xa assay: quantitative, not amenable to POC setting
81
Q

what are the point of care test that can be done to monitor UFH?

A
  • activated clotting time (ACT) test: whole blood, functional, assesses global status of pt’s blood coagulation
  • protamine titration: whole blood, quantitative, 1:1 ratio heparin to protamine
82
Q

low molecular weight heparin characteristics

A
  • half life: 3-5 hrs
  • inhibits activated factor X (Xa)
  • incomplete reversal by protamine
  • risk of bleeding is less with LMWH
  • risk of HIT may be lower
83
Q

LMWH uses

A

prevention&treatment of DVT and PE

  • unstable angina
  • myocardial infarction
  • prophylaxis in hip and knee surgery
  • interventional cardiology
84
Q

why is LMWH not appropriate for CPB

A
  • little to no anti-thrombin effect
  • not reversed with protamine
  • longer half life
85
Q

Low weight molecular heparin is only monitored in limited clinical conditions. What conditions are they?

A
  • renal insufficiency
  • pts who receive LMWH over extended periods to time such as pt with cancer or who can’t take warfarin
  • morbid obesity/very low body weight
  • very elderly, newborns, and young children
86
Q

with LMWH, when is maximum plasma concentration reached?

A

1-5 hrs post injection

87
Q

does ACT work with LMWH

A

no, does not reliably reflect level of anticoagulation

88
Q

when monitoring LMWH, what factor inhibition is measured?

A

Xa inhibition measured

89
Q

what is a common type of LMWH that we will use in cardiology?

A

Lovenox

Enoxaparin

90
Q 
Lovenox 
half life: 
route of admin: 
antidote: 
indication: 
effect on ACT:
A

LOVENOX
half life: 4.3 hrs
route of administration: IV or sub Q
antidote: protamine a 30% neutralization
indication: prophylaxis & treatment of VTE (hip/knee replacement, restricted mobility, unstable angina and non Q-wave MI)
effect on ACT: minimal to none

91
Q

What is an alternative to heparin used in cardiopulmonary bypass?

A

direct thrombin inhibitors

92
Q

what is Hirudo medicinal?

A
  • antithrombotic properties of leech saliva described in 1884
  • 1980s: leeches used for microvascular/reattachment surgery
  • 2004: FDA cleared medical device for restoration of blood flow in cosmetic and reconstructive surgery
93
Q

what do direct thrombin inhibitors, inhibit?

A

free and clot-bound thrombin

94
Q

unlike heparin, what is not required for anticoagulant actions with direct thrombin inhibitors?

A

AT3

95
Q

what are some clinical uses for Direct Thrombin Inhibitors?

A
  • cardiac Cath lab during PTCA for replacement for heparin, usually given w platelet inhibitor
  • given to its who cannot receive heparin due to antibodies against heparin (HIT)
96
Q

what are the cons of direct thrombin inhibitors?

A
  • no reversal agent

- high cost relative to heparin

97
Q

what are the direct thrombin inhibitors that are commonly used?

A
  • Angiomax Bivalirudin (synthetic)
  • Argatroban Novastan (small molecule, reversible synthetic)
  • Refludan Lepirudin
98
Q 
Angiomax Bivalirudin 
admin: 
clinical indications: 
effect on ACT: 
monitoring:
A

admin: IV, half life 36 min, cleared by kidney
clinical indications: PTCA with aspirin or other platelet inhibitor HIT
effect on ACT: prolongs
monitoring: ACT/APTT Ecarin clotting time

99
Q

Argatroban Novastan

A

admin: IV, half life 24 min, metabolized by liver
clinical indications: HIT
effect on ACT: prolongs
monitoring: ACT/APTT Ecarin clotting time

100
Q

what are some oral anticoagulants used?

A

warfarin (Coumadin)
dabigitran (Pradaxa)
rivaroxaban (Xarelto)
apixaban

101
Q

which anti coagulant was first used as rat poison

A

warfarin

102
Q

warfarin is the drug with the highest potential for (2)

A
  • clinically significant interactions with other drugs

- changes in lifestyle and dietary habits

103
Q

what is the drug that is the most frequently associated with drug related hospitalization due to bleeding or thrombotic complications

A

warfarin

104
Q

how does warfarin work?

A
  • absorbed from the GI tract and binds to ALBUMIN
  • in the liver, inhibits the enzyme required for vitamin K to carboxylate the glutamic residues of several coagulation proteins
105
Q

warfarin results in decreased levels of

A
  • 2, 7, 9, 10

- Protein C and Protein S

106
Q

how long is the onset of action following ingestion of Warfarin

A

8-12 hrs

107
Q

full anticoagulation of warfarin occurs ____ days following initiation

A

4-5 days

108
Q

clinical indications for warfarin

A
  • venous and arterial thrombosis
  • prophylaxis in patients at risk of VTE
  • prevention of thrombosis in its with fib, prosthetic heart valves, following ortho surgery
  • low dose: its with indwelling catheters for extended periods of time
109
Q

monitoring warfarin using PT/INR

A
  • 2.0 to 3.0 for all

- 2.5 to 3.5 in mechanical heart valves and cariogenic emboli

110
Q

contraindications for Warfarin

A
  • risk of hemorrhage is greater than benefits
  • pregnant/nursing moms
  • pre-existing hemorrhagic tendencies or blood dyscrasias
  • traumatic surgery with large open areas
  • recent or contemplated surgery of CNS or eyes
  • lumbar puncture/any proceed with potential for uncontrollable bleeding
111
Q

risk of non-compliance for Warfarin

A
  • senility
  • alcoholism
  • mental impairemnt/lack of patient cooperation
112
Q

when you measure PT, what is it looking at?

A

extrinsic pathway (factor 7)

113
Q

when measuring PTT, what is it looking at?

A

12, 11, 9, 8, 10

114
Q

INR stands for

A

international normalized ratios

115
Q

new oral anticoagulants (3)

A
  • dabigitran etexilate (Pradaxa)
  • rivaroxaban (Xarelto)
  • apixaban (Eliquis)
116
Q

what does Pradaxa inhibit and what does it reduce?

A
  • direct thrombin inhibitor

- reduce the risk of stroke and blood clots in its with AF, not caused by a heart valve problem

117
Q

what does Xarelto inhibit and what does it reduce?

A
  • anti-Xa inhibitor
  • reduces the risk of stroke and blood clots in pts with AF not caused by a heart valve problem
  • reduce the risk of forming a blood clot in the legs and lungs of people who have just had knee or hip replacement
118
Q

what does Xarelto treat?

A

DVT and PE

119
Q

what does Eliquis inhibit and what does it reduce?

A
  • Anti-Xa inhibitor

- reduce the risk of stroke and blood clots in its with AF not caused by a heart valve problem

120
Q

what is the difference between Xarelto and Eliquis?

A

Xarelto has a broader indication

Eliquis is very narrow and specific

121
Q

Which new oral anticoagulants deals with AF

A

Pradaxa and Eliquis

122
Q

Many people coming into surgery are going to be on

A

platelet inhibitor

123
Q

_____ has to be available at 2b3 receptor site for platelets to stay together

A

Fibrinogen

124
Q

what are two important platelet inhibitors?

A

aspirin and plavix

125
Q

aspirin characteristics

A 
MOA: cycle-oxygenase inhibition 
half life: 2-3 hrs 
length of effect: permanent 
Admin Route: oral 
effect on ACT: none
126
Q

plavix characteristics

A 
MOA: ADP inhibition 
half life: 8 hrs 
length of effect: permanent 
admin route: oral 
effect on ACT: none
127
Q

when do you stop plavix if you are going to have surgery?

A

7-10 days before surgery

128
Q

Thombolytic agents can be thought of as……

A

THE CLOT BUSTERS!!!

129
Q

when you see a word ending in -ase, that means

A

to break up a clot

130
Q

does heparin break up clots?

A

NO

heparin does not stop clots, it slows it down

131
Q

what is a major complication with thrombolytic agents?

A

bleeding

especially intracranial

132
Q

what are the thombolytic agents? (3)

A

streptokinase

urokinase

tissue plasminogen activator (TPA)

133
Q

Streptokinase characteristics (3)

A
  • derived from group C, b-hemolytic streptococci
  • not fibrin specific
  • antigenicity makes retreatment difficult
134
Q

urokinase (Abbokinase) characteristics

A
  • derived from cultured human cells (renal)

- not Fibrin specific

135
Q

Tissue Plasminogen Activator (TPA) characteristics (3)

A
  • recombinant from human cells
  • fibrin specific
  • alteplase, Reteplase (rPA), tenecteplase
136
Q

what are the antifibrinolytic agents

A

EACA (Amicar)
tranexamic acid (Cyclokapron)
Aptoinin (trasylol)

137
Q

what is important to remember about antifibrinolytic agents?

A

inhibits plasminogen

138
Q

Epsilon Amino Caproic Acid (Amicar) characteristics

A

inhibits activators of plasminogen

139
Q

Tranexamic acid (cyclokapron)

A

inhibits activation of plasminogen

140
Q

aprotinin (trasylol)

A
  • serine protease inhibitor
  • inhibits factor XIIa, kvllikrein, plasmin generator by TPA
  • inhibits systemic inflammatory response
  • no longer on market
141
Q

what do you give when a pt won’t stop bleeding

A

Recombinant Factor VIIa

  • novoSeven
  • powerful drug to clot everything off
142
Q

indications for use for Recombinant Factor VIIa NovoSeven

A
  • hemophilia A and B patients who have developed antibodies to Factor VIII/IX
  • treatment of bleeding episodes in FVII deficiency
  • prevention of bleeding in surgical procedures for both inhibitor pts and FVII-deficient pts
  • treament of acquired hemophilia
143
Q

why would someone have a factor VII deficiency?

A

because of Warfarin

144
Q

off label use of Recombinant factor VIIa NovoSeven

A
  • liver transplantation
  • acute intra-cerebral hemorrhage
  • trauma
  • rescue intervention for intractable bleeding where other measures have failed
145
Q

what is a risk for using recombinant factor VIIa NovoSeven?

A

risk of DIC and thromboembolic events

Coagulation (5 decks)

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