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Coag Assessment Final > Coag > Flashcards

Coag Flashcards

1
Q

What happens in Primary Hemostasis?

A

Platelet deposition at injury site

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2
Q

What is formed during Primary Hemostasis?

A

Initial platelet plug

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3
Q

What is Secondary Hemostasis?

A

Clotting factors activated

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4
Q

What stabilizes the clot in Secondary Hemostasis?

A

Crosslinked fibrin

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5
Q

What process is involved in secondary hemostasis?

A

Coagulation

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6
Q

What activates fibrin in the clotting process?

A

Factor Ia

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7
Q

What are some anti-clotting mechanisms of vascular endothelial cells?

A

Negatively charged, produce platelet inhibitors, excrete adenosine diphosphatase, increase protein C, produce TFPI, synthesize t-PA

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8
Q

What does vascular endothelial cells excrete to degrade adenosine diphosphate (ADP)?

A

Adenosine diphosphatase

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9
Q

What is the anticoagulant produced by vascular endothelial cells to inhibit factor Xa & TF-VIIa complex?

A

Tissue Factor Pathway Inhibitor (TFPI)

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10
Q

Where are platelets derived from?

A

Bone-marrow megakaryocytes

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11
Q

What is the lifespan of nonactivated platelets? How many new platelets are formed daily under normal conditions?

A

8 to 12 days.

1.2−1.5 × 10^11

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12
Q

What is present in the platelet membrane that increases surface area?

A

Surface canalicular system

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13
Q

What is exposed when there is damage to endothelium?

A

ECM containing collagen and platelet-adhesive glycoproteins

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14
Q

What are the 3 phases of alteration that platelets undergo upon exposure to ECM?

A

adhesion, activation, aggregation

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15
Q

What occurs when platelets interact with collagen and tissue factor?

A

Activation

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16
Q

What do alpha granules contain?

A

Fibrinogen, factors V & VIII, vWF, PDGF

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17
Q

What do dense bodies contain?

A

ADP, ATP, calcium, serotonin, histamine

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18
Q

What promotes fibrin crosslinking during aggregation?

A

Activated glycoprotein IIb/IIIa receptors

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19
Q

What is required for each stage of the cascade?

A

Membrane-bound activation tenase-complexes

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20
Q

What does each complex consist of?

A

Substrate, enzyme, cofactor, calcium

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21
Q

What is the Extrinsic Pathway?

A

Initiation phase of plasma-mediated hemostasis

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22
Q

What is formed when TF binds to VIIa?

A

TF/VIIa complex

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23
Q

What does the TF/VIIa complex activate?

A

Factor X

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24
Q

What does the TF/VIIa complex also activate in the intrinsic pathway?

A

IX→ IXa

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25
Q

What converts factor X to Xa in the intrinsic pathway?

A

IXa and calcium

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26
Q

Which factor begins the final common pathway?

A

Factor Xa

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27
Q

How was the intrinsic pathway initially thought to occur?

A

Thought to occur only in response to endovascular contact with negatively charged substances

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28
Q

What is the current understanding of the intrinsic pathway?

A

Amplification system to propagate thrombin generation initiated by extrinsic pathway.

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29
Q

What is the first step in intrinsic pathway hemostasis initiation?

A

Upon contact with negatively charged surface, Factor XII is activated

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30
Q

What converts XI to XIa in the intrinsic pathway?

A

Factor XIIa

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31
Q

Which components convert factor X to Xa in the intrinsic pathway?

A

XIa + VIIIa + plt-membrane phospholipid + Ca++

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32
Q

What initiates the final common pathway in the intrinsic pathway?

A

Xa

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33
Q

What does activated thrombin (IIa) do in the intrinsic pathway propagation?

A

Activates factors V, VIII, and XII to amplify extrinsic thrombin generation

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34
Q

What leads to the propagation of the final common pathway in hemostasis?

A

Platelet activation

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35
Q

What does Factor X become in the common pathway?

A

Xa

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36
Q

What does Xa bind with to form the prothrombinase complex”?”

A

Va

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37
Q

What is rapidly converted into thrombin by the prothrombinase complex?

A

prothrombin (II)

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38
Q

What does thrombin convert fibrinogen (I) into?

A

fibrin (Ia)

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39
Q

What stabilizes the clot by forming a mesh?

A

Fibrin molecules crosslink to form a mesh that stabilizes the clot.

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40
Q

Thrombin cleaves__________ from fibrinogen to generate __________?

A

Fibrinopeptides A & B
Fibrin Monomers

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41
Q

What crosslinks the fibrin strands to stabilize and form an insoluble clot?

A

Factor XIIIa

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42
Q

What is the key-step in regulating hemostasis?

A

Thrombin generation

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43
Q

What does the Common Pathway depict?

A

Thrombin generation and fibrin formation

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44
Q

Which complexes facilitate the formation of prothrombinase complexes?

A

Both intrinsic and extrinsic tenase-complexes

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45
Q

What components make up the Intrinsic Tenase Complex?

A

Activator, IXa, VIIIa, Ca²

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46
Q

What components make up the Extrinsic Tenase Complex?

A

Injury, TF, VIIa, Ca²

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47
Q

What are the three Serine Protease Inhibitors (SERPINs)

A

Antithrombin, Heparin and Heparin cofactor II

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48
Q

What is the role of fibrinolysis in anticoagulation?

A

endovascular TPA and urokinase convert plasminogen to plasmin

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49
Q

How does Plasmin contribute to anticoagulation?

A

Plasmin breaks down clots enzymatically and Degrades factors V & VIII

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50
Q

What does Tissue Factor Pathway Inhibitor (TFPI) do in anticoagulation?

A

Forms complex with Xa that Inhibits TF/7a complex along with Xa. This down-regulates the extrinsic pathway.

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51
Q

How does the Protein C system contribute to anticoagulation?

A

Inhibits factors II, Va, VIIIa

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52
Q

What is the role of Antithrombin (AT) in anticoagulation?

A

Inhibits thrombin and factor IXa, Xa, XIs and XIIa

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53
Q

How does Heparin enhance anticoagulation?

A

Heparin binds to Antithrombin and accelerates Antithrombin activity

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54
Q

What does Heparin cofactor II do in anticoagulation?

A

Inhibits thrombin alone

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55
Q

Why is preop identification and correction of hemostatic disorders vital?

A

Predicts bleeding risk

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56
Q

What is the most effective predictor of bleeding in preop assessment?

A

Carefully performing a Bleeding history is the most effective predictor of bleeding

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57
Q

What should be inquired about in a bleeding history for preop assessment?

A

Nose bleeds, bleeding gums, easy bruising

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58
Q

What should be asked about regarding excessive bleeding in preop assessment?

A

Dental extractions, surgery, trauma, childbirth, blood transfusion

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59
Q

What medications should be asked about in preop assessment?

A

Blood thinners: ASA, NSAIDs, vitamin E, Ginko, Ginger, Garlic

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60
Q

What coexisting disorders should be considered in preop assessment?

A

Renal, liver, thyroid, bone marrow disorders.

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61
Q

What are the standard first-line labs if a bleeding disorder is suspected?

A

PT, aPTT

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62
Q

What are some causes of bleeding disorders?

A

Von Willebrand’s, Hemophilia, Drug-induced bleeding, Liver disease, Chronic renal disease, Disseminated Intravascular Coagulation and Trauma-induced coagulopathy

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63
Q

What is the role of vWF?

A

It plays a critical role in platelet adhesion and prevents degradation of factor VIII

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64
Q

What is the most common inherited bleeding disorder? What percent of the population are affected by this dz?

A

Von Willebrand’s Disease
1% of population

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65
Q

What are the main characteristics of Von Willebrand’s Disease?

A

Deficiency in vWF, causing defective plt adhesion/aggregation

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66
Q

Why might routine coagulation labs not be helpful in diagnosing Von Willebrand’s Disease?

A

Platelets & PT will be normal; aPTT might be prolonged d/o level of factor 8

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67
Q

What are the better tests for diagnosing Von Willebrand’s Disease?

A

vWF level, vWF-plt binding activity, Factor 8 level, Plt function assay

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68
Q

How is mild von Willebrand’s Disease often managed?

A

Responsive to DDAVP (↑s vWF)

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69
Q

What may be required for intraoperative bleeding in Von Willebrand’s Disease?

A

Administration of vWF & Factor 8 concentrates

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70
Q

What is Hemophilia A? What is the incidence of Hemophilia A?

A

Factor 8 deficiency

1 in 5,000

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71
Q

What is Hemophilia B? What is the incidence rate of Hemophilia B?

A

Factor IX deficiency

1 in 30,000

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72
Q

How much of hemophilia cases are genetically inherited? What is the cause of the other 1/3 cases?

A

2/3
1/3-present as new mutations

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73
Q

When does hemophilia often present? What are the presenting signs?

A

Frequently presents in childhood as spontaneous hemorrhage in joints & muscles

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74
Q

What do the lab results show in hemophilia?

A

Normal PT, Plts, bleeding time; prolonged PTT

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75
Q

Who should be consulted preoperatively for hemophilia?

A

Hematologist

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76
Q

What may be indicated before surgery in hemophilia?

A

DDAVP and Factors 8/9

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77
Q

List the pharmacological anticoagulation drugs that a CRNA must be aware of?

A

Heparin, warfarin, Direct Oral Anticoags (DOACs), Beta-lactam abx, Nitroprusside, NTG, NO, SSRIs.

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78
Q

What is the most significant cause of intraoperative bleeding?

A

Anticoagulant meds

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79
Q

What must a CRNA understand regarding anticoagulant drugs?

A

Pharmacodynamics and how to reverse them

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80
Q

What are the primary coagulation factors synthesized by the liver?

A

Factors V, VII, IX, X, XI, XII

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81
Q

Besides coagulation factors, what other proteins are synthesized by the liver?

A

Protein C & Proteins S, antithrombin

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82
Q

What hemostatic issues can occur in liver disease?

A

Impaired synthesis of coagulation factors
Quantitative and qualitative platelet dysfunction
Impaired clearance of clotting and fibrinolytic proteins

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83
Q

What lab findings are often seen in liver disease in relation to clotting tests?

A

Prolonged PT and possible prolonged PTT

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84
Q

Why might traditional clotting tests not fully represent the coagulation status in liver disease?

A

Values only reflect lack of pro-coagulation factors, not accounting for lack of anticoagulation factors

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85
Q

How do chronic liver patients usually display hemostasis despite their condition?

A

Rebalanced hemostasis with sufficient thrombin production

86
Q

Are chronic liver patients prone to disruptions in coagulation despite having a rebalanced hemostasis?

A

Yes, susceptible to disruption in coagulation

87
Q

What other coagulation tests can be useful in the context of liver disease?

A

TEG & ROTEM

88
Q

What is the cause of baseline anemia in CKD patients?

A

Lack of erythropoietin and platelet dysfunction (due to uremic environment)

89
Q

How can dialysis and correction of anemia impact bleeding times in CKD patients?

A

Shorten bleeding times

90
Q

What are treatment options for platelet dysfunction in CKD patients?

A

Cryoprecipitate, DDAVP, Conjugated estrogens

91
Q

What is Disseminated Intravascular Coagulation?

A

Pathological hemostatic response to TF/7a complex, which causes excessive activation of the extrinsic pathway.

92
Q

How does excessive activation of the extrinsic pathway in DIC increase bleeding?

A

The excessive activation of extrinisic pathway overwhelms the anticoagulation mechanisms and generates intravascular thrombin.

93
Q

What causes depletion of coagulation factors and platelets in DIC?

A

Widespread microvascular thrombotic activity

94
Q

What can precipitate DIC?

A

Trauma, amniotic fluid embolus, malignancy, sepsis, incompatible blood transfusion

95
Q

What are some lab findings in DIC?

A

↓Plts, prolonged PT/PTT/Thrombin time, ↑soluble fibrin & fibrin degradation products

96
Q

How should DIC be managed?

A

Correct underlying condition, administration of appropriate blood products

97
Q

What is a common cause of trauma-related death?

A

Uncontrolled hemorrhage

98
Q

What are the causes of coagulopathies in trauma?

A

Acidosis, hypothermia, hemodilution

99
Q

What is Trauma Induced Coagulopathy (TIC)?

A

Independent acute coagulopathy in trauma pts. This is thought to be related to activated protein C decreasing thrombin generation.

100
Q

What is thought to be the driving factor for protein C activation in TIC?

A

Hypoperfusion

101
Q

How does the degradation of proteoglycan-containing endothelial glycocalyx in TIC cause excessive bleeding?

A

Proteoglycan-shedding results in auto-heparinization

102
Q

What also contributes to the increased bleeding in TIC?

A

Platelet dysfunction

103
Q

The most common inherited prothrombotic disease is caused by a mutation of ___________?

A

Factor V Leiden or PT

104
Q

What does Factor V Leiden mutation lead to?

A

Activated protein C resistance

105
Q

What percentage of the Caucasian population has the Factor V Leiden mutation?

A

5%

106
Q

What does the prothrombin mutation cause?

A

↑PT concentration leading to hypercoagulation

107
Q

What does thrombophilia refer to?

A

Inherited or acquired predisposition for thrombotic events

108
Q

How does thrombophilia generally manifest?

A

Venous thrombosis

109
Q

What are individuals with prothrombotic states highly susceptible to?

A

Virchow’s Triad

110
Q

What are the components of Virchow’s Triad

A

blood stasis, endothelial injury, hypercoagulability

111
Q

What is Antiphospholipid Syndrome?

A

autoimmune disorder with antibodies against the phospholipid-binding proteins in the coagulation system.

112
Q

What is Antiphospholipid Syndrome characterized by?

A

Recurrent thrombosis and pregnancy loss

113
Q

What is one of the treatments often required for patients with Antiphospholipid Syndrome?

A

Life-long anticoagulants

114
Q

What factors greatly increase the risk of thrombosis in individuals with Antiphospholipid Syndrome?

A

Oral contraceptives, pregnancy, immobility, infection, surgery & trauma

115
Q

What is HIT and when does it usually occur?

A

HIT is Mild-moderate thrombocytopenia associated with Heparin. Usually occurs 5-14 days after heparin tx

116
Q

What can Heparin-Induced Thrombocytopenia result in?

A

Platelet count reduction, activation of remaining platelets, and potential thrombosis

117
Q

What is a risk factor for Heparin-Induced Thrombocytopenia?

A

Women, high heparin doses such as with cardiopulmonary bypass. Unfractionated heparin has greater risk than LMWH.

118
Q

What should be done if HIT is suspected?

A

D/C heparin, convert to alternative anticoagulant

119
Q

What anticoagulant is contraindicated with HIT and why?

A

Warfarin is contraindicated since it decreases Protein C and Protein S synthesis.

120
Q

How is HIT diagnosis confirmed?

A

HIT antibody testing

121
Q

How long do HIT antibodies remain in circulation?

A

Typically cleared from circulation in 3 months.

122
Q

What does Prothrombin Time (PT) assess?

A

Integrity of extrinsic & common pathways

123
Q

Which factors’ deficiencies does PT reflect?

A

1, 2, 5, 7, 10 (II, V VII, X)

124
Q

What is used to monitor Vitamin K antagonists like Warfarin?

A

PT. Factors II, VII and X are vit K dependent.

125
Q

What does aPTT assess?

A

Intrinsic and common pathway.

126
Q

What is Activated Partial Thromboplastin Time (aPTT) sensitive to?

A

Deficiencies in factor 8 & 9 (VIII, IX)

127
Q

What can aPTT measure the effect of?

A

Heparin

128
Q

What does the Anti-factor Xa activity assay assess?

A

Functional assessment of Heparin’s anticoagulant effect.
Can also be used to assess LMWH, Fondaparinux, and factor Xa inhibitors.

129
Q

What is the purpose of the Platelet Count test? What is the normal Platelet count?

A

Coagulation testing
normal platelet count >100,000 platelets/microliter

130
Q

What does the Activated Clotting Time (ACT) measure? What is the normal ACT result?

A

Addresses intrinsic and common pathways, it is used to assess responsiveness to heparin.
Normal 107 +/- 13 seconds.

131
Q

What is the most popular point-of-care method to determine perioperative heparin concentration?

A

Protamine-concentration

132
Q

How does 1mg protamine affect 1mg heparin?

A

Inhibit

133
Q

What happens to the time to clot as increasing amounts of protamine are added to heparinized blood?

A

Decreases until protamine concentration > heparin concentration

134
Q

What do Viscoelastic Coagulation Tests measure?

A

All aspects of clot formation from early fibrin generation to clot retraction and fibrinolysis. Coagulation diagrams are generated as a result of this test.

135
Q

What are the benefits of TEG and ROTEM?

A

They allow for more precise blood product administration.

136
Q

What is the normal range for R time on a thromboelastogram (TEG)?

A

5 - 10 minutes

137
Q

What does the Alpha angle represent on a thromboelastogram (TEG)?

A

Maximum amplitude

138
Q

What is MA in a thromboelastogram (TEG)?

A

Highest vertical amplitude

139
Q

What does LY30 measure on a thromboelastogram (TEG)?

A

Percentage of amplitude reduction 30 minutes after maximum amplitude

140
Q

What is the treatment for excess fibrinolysis on a thromboelastogram (TEG)?

A

Tranexemic Acid and/or Aminocaproic Acid

141
Q

What do antiplatelet agents do?

A

Inhibit platelet aggregation and/or adhesion

142
Q

What are the 3 main classes of Antiplatelet Agents?

A

COX Inhibitors, P2Y12 receptor antagonists, Platelet GIIb/IIIa Receptor antagonists.

143
Q

What do Cyclooxygenase Inhibitors block in platelet aggregation?

A

Block Cox 1 from forming TxA₂

144
Q

How long do the antiplatelet effects of ASA and NSAIDs last after discontinuation?

A

ASA: 7-10 days
NSAIDs: 3 days

145
Q

How do P2Y12 receptor antagonists work?

A

Inhibit P2Y12-R, preventing GIIb/IIIa expression

146
Q

What is the duration of antiplatelet effects for Clopidogrel after discontinuation? Ticlopidine? Ticagrelor and Cangrelor?

A

Clopidogrel: 7 days
Ticlopidine: 14-21 days
Ticagrelor and Cangrelor: Short-acting <24 hours

147
Q

What do Platelet GIIb/IIIa receptor antagonists prevent?

A

vWF & fibrinogen from binding to GIIb/IIIa-R

148
Q

Name three Platelet GIIb/IIIa receptor antagonists.

A

Abciximab, Eptifibatide, Tirofiban

149
Q

What do Vitamin K antagonists inhibit the synthesis of?

A

Vit-K dependent factors 2, 7, 9, 10, Protein C & S

150
Q

What is the most common Vitamin K antagonist?

A

Warfarin

151
Q

What is the drug of choice for valvular Afib and valve replacements?

A

Warfarin

152
Q

How long does it take for Warfarin to reach therapeutic INR (2-3)?

A

3-4 days due to long half-life of 40 hours.

153
Q

What is often required until Warfarin reaches its therapeutic effect?

A

Heparin

154
Q

What lab tests are frequently required for monitoring Warfarin therapy?

A

PT/INR

155
Q

How can Warfarin’s anticoagulant effects be reversed?

A

Vitamin K

156
Q

What is the mechanism of action of Heparin?

A

Binds to antithrombin, inhibits thrombin and Xa

157
Q

What are some characteristics of Unfractionated Heparin?

A

Short half-life, given IV
Fully reversed with Protamine
Close monitoring required

158
Q

What are the characteristics of LMWH?

A

longer half-life, dosed BID SQ
No coag test needed
Protamine only partially effective with LMWH

159
Q

What is half-life of Fondaprinux? How often is Fondaparinux dosed?

A

Much longer half-life (17-21 hours) therefore it is dosed Once a day
*protamine ineffective

160
Q

What is the mechanism of Direct Thrombin Inhibitors?

A

Bind/block thrombin in both soluble & fibrin-bound states

161
Q

What is the natural source of Hirudin?

A

Leeches

162
Q

What are some characteristics of Argatroban?

A

synthetic, reversibly binds to thrombin.
Half-life 45 mins.
Monitored intraop with PTT or ACT

163
Q

What are some characteristics of Bivalirudin?

A

Bivalirudin is the synthetic Direct Thrombin Inhibitor that has the shortest half-life
DOC for renal/liver impairment

164
Q

What is Dabigatran (Pradaxa)?

A

1st DOAC
DTI approved for CVA prevention and non-valvular A-fib

165
Q

What are the key advantages of DOACs over Warfarin?

A

More predictable pharmacokinetics/dynamics, fewer drug interactions, fewer embolic events, fewer intracranial hemorrhages, lower mortality than heparin, dosed daily without lab monitoring

166
Q

What is the efficacy of DOACs compared to Warfarin?

A

Similar efficacy with much shorter half-life

167
Q

Name a Direct Thrombin Inhibitor.

A

Dabigatran (Pradaxa)

168
Q

Name three Direct Xa Inhibitors.

A

Rivaroxaban (Xarelto), Apixaban (Eliquis), Edoxaban (Savaysa)

169
Q

What is the primary use of Thrombolytics? How are these drugs administered?

A

To dissolve blood clots
IV or directly into site of blockage.

170
Q

What is the mechanism of action for most Thrombolytics?

A

Most of Serine Proteases that convert plasminogen to plasmin, breaking down fibrinogen to fibrin

171
Q

Name a Fibrin-Specific Thrombolytic.

A

Altepase (tPA), Reteplase, Tenecteplase

172
Q

Name a Non-Fibrin-Specific Thrombolytic. Why is this drug not commonly used?

A

Streptokinase. Decreased use due to allergic reactions.

173
Q

Why is Streptokinase not widely used?

A

Allergic reactions

174
Q

What are the concerns with surgery for patients on thrombolytics?

A

Surgery contraindicated within 10 days of thrombolytic treatment

175
Q

What are some absolute contraindications for thrombolytics?

A

Vascular lesions, Severe, uncontrolled hypertension, Recent cranial surgery or trauma, Brain tumor, Ischemic stroke <3 months prior, Active bleeding

176
Q

What are some relative contraindications for thrombolytics?

A

Ischemic stroke >3 months prior, Active peptic ulcer, Current use of anticoagulant drugs, Pregnancy, Prolonged/traumatic CPR <3 weeks prior, Major surgery <3 weeks prior

177
Q

What is the benefit of procoagulants?

A

They mitigate blood loss

178
Q

What are the two classes of procoagulants used to mitigate blood loss?

A

Antifibrinolytics & Factor Replacements

179
Q

What are the two subclasses of antifibrinolytics?

A

Lysine analogues & SERPIN

180
Q

Name two lysine analogues used as antifibrinolytics. What are lysine analogues MOA?

A

Epsilon-amino-caproic acid (EACA) & Tranexamic Acid (TXA)
MOA: Binds & inhibits plasminogen from binding to fibrin, impairing fibrinolysis

181
Q

What class of drugs does Aprotinin belong to? Why was it removed from the market?

A

Aprotinin is a Serine protease inhibitor (SERPIN). Renal & cardio toxicity

182
Q

List the 5 Factor replacements

A

Recombinant VIIa, Prothrombin complex Concentrate (PCC), Fibrinogen Concentrate, Cryoprecipitate and FFP

183
Q

What does Recombinant VIIa (RfVIIa) do in factor replacements?

A

Increases thrombin generation via intrinsic & extrinsic paths

184
Q

What does Prothrombin Complex Concentrate (PCC) contain?

A

Vitamin-K factors

185
Q

What is Fibrinogen Concentrate derived from?

A

Pooled plasma

186
Q

Why might Cryoprecipitate & FFP be preferable to more specific coag factor replacements?

A

Cheaper & contain more coag factors, but less specific composition

187
Q

When should low risk patients discontinue warfarin before surgery? When should they restart warfarin?

A

D/C: 5 days prior to surgery
Restart: 12-24 hours post op

188
Q

When should high risk patients discontinue warfarin before surgery? When should they restart warfarin?

A

D/C: 5 days prior to surgery.
They should not restart warfarin but rather bridge with unfractionated heparin or LMWH.

189
Q

How should unfractionated heparin be managed pre-surgery?

A

d/c: 4-6h prior
Restart: no bolus, greater than or equal to 12 hours post op

190
Q

When should LMWH be discontinued before surgery?

A

D/C: 24h prior to surgery
Restart: 24 hour post op

191
Q

What is the guideline for aspirin use in moderate to high risk patients pre-surgery?

A

Continue

192
Q

When should low risk patients stop aspirin before surgery?

A

7-10 days

193
Q

How long to delay elective surgery after bare-metal stent placement?

A

6 weeks

194
Q

How long to delay elective surgery after drug-eluding stent placement?

A

6 months

195
Q

When is warfarin reversal indicated?

A

Excessive bleeding ro emergent surgery

196
Q

What is the drug of choice for emergent coumadin reversal?

A

Prothrombin Complex Concentrates

197
Q

What must be given concurrently when reversing warfarin?

A

Vitamin K must be given concurrently to restore carboxylation of vit K dependent factors by the liver for more sustained correction.

198
Q

Why are direct thrombin inhibitors more difficult to reverse?

A

Most don’t have a reversal. The exception being Dabigatran (Pradaxa)

199
Q

What is the antidote for Dabigatran (Pradaxa)?

A

Idarucizumab

200
Q

How can Factor Xa Inhibitors be reversed?

A

Andexanet, a derivative of factor Xa

201
Q

Reversal agent for ASA

A

Platelet transfusion

202
Q

Reversal agent for P2Y12 receptor antagonists

A

GPIIb/IIIa antagonists

203
Q

Stop before procedure days for P2Y12 receptor antagonists

A

7-14 days

204
Q

Monitoring required for Warfarin

A

PT, INR

205
Q

Reversal agents for Warfarin

A

PCC, FFP, vitamin K

206
Q

Monitoring required for Unfractionated Heparin (UFH)

A

aPTT

207
Q

Reversal agent for UFH

A

Protamine

208
Q

Monitoring recommended for Low-molecular weight heparin (LMWH)

A

fXa levels

209
Q

Reversal agent for LMWH

A

Partially reversed by protamine

210
Q

Monitoring recommended for Fondaparinux

A

fXa levels

211
Q

Monitoring required for Argatroban, Bivalirudin

A

aPTT or ACT

212
Q

Reversal agent for Rivaroxaban and Apixaban

A

Andexanet alfa

Coag Assessment Final (1 decks)

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