Coagulation (4) Flashcards

1
Q

How does hemostasis normally control bleeding?

A

Balance btw clot generation, thrombus formation, andregulatory mechanisms that inhibit uncontrolled thrombogenesis

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2
Q

What are the goals of hemostasis?

A
  • Limit blood loss from vascular injury
  • Maintain intravascular blood flow
  • Promote revascularization after thrombosis
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3
Q

What are the 2 stages of hemostasis?

A
  • Primary homeostasis
  • Secondary homeostasis
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4
Q

What is primary hemostasis?

A
  • Immediateplatelet deposition at the endovascular injury site
  • Leads to the initial platelet plug formation
  • Only adequate for minor injury
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5
Q

What is secondary homeostasis?

A
  • Clotting factors activated
  • Stabilized clot formed and secured with crosslinked fibrin
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6
Q

What is the role of vascular endothelial?

A
  • antiplatelet, anticoagulant, and fibrinolytic effects to inhibit clot formation
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7
Q

How do vascular endothelial cells function as an antiplatelet?

A
  • Endothelial cells are negatively charged to repel platelets
  • Produce platelet inhibitors such as prostacyclin and nitric oxide
  • Excrete adenosine diphosphatase
  • Increase protein C
  • Produce tissue factor pathway inhibitor
  • Synthesize tPA
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8
Q

What is the function of adenosine diphosphate?

A

Degrades adenosine diphosphate (ADP), a platelet activator

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9
Q

What is the MOA of tissue factor pathway inhibitor?

A

Inhibits factor Xa & TF-VIIa complex

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10
Q

What are platelets derived from?

A

Bone-marrow megakaryocytes

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11
Q

What are the characteristics of inactive platelets?

A
  • Disc shaped
  • Anuclear (no nucleus)
  • 8-12 day lifespan
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12
Q

Approximately ____% of platelets are consumes to support vascular integrity

A

10%

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13
Q

_________ new platelets are formed daily

A

120-150 billion

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14
Q

What is the function of the platelet membrane?

A
  • Contains numerous receptors
  • Surface canalicular system → increases membrane surface area
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15
Q

How does damage to endothelium signal for clotting cascade?

A

Damaged endothelium exposes underlying extracellular matrix (ECM): contains vWF, collagen, glycoproteins

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16
Q

What happens to platelets when extracellular matrix is exposed?

A

3 phases of alteration:
- Adhesion
- Activation
- Aggregation

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17
Q

When does platelet activation occur?

A
  • Stimulated when platelets interact with collagen and tissue factor
  • Causes release of granular contents
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18
Q

What are the 2 types of granules that platelets contain?

A
  • Alpha granules: contain fibrinogen, factors V & VIII, vWF, Plt-derived growth factor & more
  • Dense bodies: contain ADP, ATP, calcium, serotonin, histamine, epinephrine
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19
Q

When does platelet aggregation occur?

A

When the granular contents are released→ activate additional platelets and propagate plasma-mediated coagulation

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20
Q

Each stage of the clotting cascade requires assembly of membrane bound activated __________ complexes

A

Tenase

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21
Q

What is each activated tenase-complex composed of?

A
  • Substrate (Inactive)
  • Enzyme (activated coag factor)
  • Cofactor (accelerator of catalyst)
  • Calcium
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22
Q

The _________ pathway is the initiation phase of plasma mediated hemostasis

A

Extrinsic

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23
Q

What are steps of the extrinsic pathway?

A

1) Endothelial injury→ expose tissue factor to plasma
2) Tissue factor/VIIa complex
3) TF/VIIa complex binds and activates Factor X→ becomes Xa (activated)
4) TF/VIIa also activates IX→IXa
5) IXa and calcium convert X →Xa (intrinsic pathway)
6) Xa starts the common pathway

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24
Q

What factor is the start of the common pathway?

A

Factor Xa

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25
Q

What factor starts the intrinsic pathway?

A

Factor XIIa

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26
Q

What is the role of the intrinsic pathway?

A
  • Minor role in the initiation of homeostasis
  • Functions as an AMPLIFICATION system→ propagate thrombin generation initiated from extrinsic path
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27
Q

Most thrombotic events follow ___________ pathway

A

Extrinsic

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28
Q

Lab coag studies rely on _________ pathway to activate the cascade (hemostasis initiation)

A

Intrinsic

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29
Q

Explain how intrinsic pathway initiated hemostasis:

A

1) Factor XII is activated when it contacts (-) charged endothelial cells
2) Factor XIIa converts XI→XIa
3) XIa + VIIIa + plt membrane + Ca2+: converts X→Xa
4) Xa initiates final common pathway

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30
Q

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

A
  • XIa
  • VIIIa
  • plt-membrane phospholipid
  • Ca++
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31
Q

The intrinsic pathway activates thromin (IIa) which activates which factors?

A
  • Factor V
  • Factor VII
  • Factor VIII
  • Factor XI

all these factors amplify thrombin generation and activates platelets to lead to common pathway

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32
Q

What happens in the common pathway?

A

1) Factor X→Xa
2) Xa binds with Va→ prothrombinase complex
3) Prothrombinase complex converts Prothrombin (II)→ thrombin (IIa)
4) IIa attaches to plts and converts fibrinogen (I)→ fibrin (Ia)
5) Fibrin crosslink to form mesh/stabilize clot

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33
Q

What is the function of thrombin?

A
  • Converts fibrinogen (I) to Fibrin (Ia)
    (Cleaves fibrinopeptides from fibrinogen to generate fibrin)
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34
Q

How does fibrin form a stabilized clot?

A

Fibrin polymerizes into strands to form a basic clot

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35
Q

Which factor crosslinks the fibrin strands to stabilize and make an insoluble clot that is resistant to fibrinolytics?

A

Factor XIIIa

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36
Q

_________ generation is the key-step in regulating hemostasis

A

Thrombin

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37
Q

Both intrinsic and extrinsic tenase complexes facilitate the formation of __________ __________

A

Prothrombinase complexes

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38
Q

What are the 4 major coagulation counter-mechanisms?

A
  • Fibrinolysis
  • Tissue factor pathway inhibitor (TFPI)
  • Protein C
  • Serine protease inhibitors (SERPINs)
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39
Q

What is the MOA of fibrinolysis?

A
  • TPA and urokinase→ convert plasminogen to plasmin which breaks down the clot enzymatically
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40
Q

Which factors does plasmin degrade?

A

Factor V and VIII

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41
Q

What is the MOA of tissue factor pathway inhibitor?

A

Forms complex with Xa→ inhibits tissue factor/VIIa complex, Xa, and downregulates the extrinsic pathway

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42
Q

What is the MOA of protein C?

A

Inhibits factors:
- 2
- 5
- 8

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43
Q

What are examples of serine protease inhibitors?

A
  • Antithrombin
  • Heparin
  • Heparin Cofactor II
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44
Q

What factors does an antithrombin inhibit?

A
  • Thrombin
  • 9, 10, 11, 12
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45
Q

What is the MOA of heparin and what factors does heparin inhibit?

A
  • Binds to antithrombin causing conformational change
  • accelerates antithrombin
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46
Q

What is MOA of heparin cofactor II?

A

Inhibits thrombin alone

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47
Q

What test is the most effective predictor of bleeding?

A

Bleeding time

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48
Q

What should be asked about to assess bleeding risk in preop?

A
  • Nose bleeds
  • Bleeding gums
  • easy bruising
  • excessive bleeding w/dental extraction
  • excessive bleeding with past surgery
  • trauma
  • childbirth
  • blood transfusions
  • fam hx
  • use of blood thinners
  • co-morbidities (liver, renal, thyroid, bone marrow disorders)
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49
Q

What should you do if you suspect bleeding disorder?

A

PT and aPTT are standard first-line labs

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50
Q

What is the most common inherited bleeding disorder?

A

Von Willebrands Disease: effects 1% of population

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51
Q

What lab tests are good for detecting vWD?

A
  • vWF level
  • vWF plt binding activity
  • Factor 8 level
  • Plt function test
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52
Q

What is a common medical treatment for mild vWD?

A

DDAVP (increases vWF)

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53
Q

If a patient with vWD has intraop bleeding, what way be required?

A

vWF administration and factor 8 concentrates

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54
Q

vWF plays a critical role in platelet adhesion and prevents degradation of factor ____.

A

8

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55
Q

What is hemophilia A?

A

Factor 8 deficiency
occurs 1:5,000

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56
Q

What is hemophilia B?

A

Factor 9 deficiency
Occurs 1: 30,000

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57
Q

Is hemophilia genetic?

A
  • 2/3 genetic
  • 1/3 mutation with no family history
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58
Q

How does hemophilia usually present?

A

In childhood as spontaneous hemorrhage involving joints and muscles

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59
Q

What do labs show with hemophilia?

A
  • Normal PT, Plt, and bleeding time
  • PTT prolonged
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60
Q

What can be used in preop to prophylactically treat patient with hemophilia?

A
  • DDAVP
  • Factor 8
  • Factor 9
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61
Q

______ meds are the most significant cause of intraoperative bleeding

A

Anticoagulants

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62
Q

What herb can prolong bleeding time?

A

Garlic
* d/c 7-10 days before surgery

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63
Q

Common herbs/supplements that impact bleeding risk:

A
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64
Q

The liver is the primary source of which factors?

A

5, 7, 9, 10, 11, 12

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65
Q

How does liver disease lead to hemostatic issues?

A
  • Impaired coagulation factor synthesis
  • Platelet dysfunction (quantity and quality)
  • Impaired clearance of clotting and fibrinolytic proteins
66
Q

What are common lab findings in pts with liver disease?

A
  • Prolonged PT
  • possible prolonged PTT

Only accounting for lack of pro-coagulation factors no accounting for lack of anticoagulation factors

67
Q

Do chronic liver patients suffer from insufficient thrombin production?

A

No, they often have rebalanced hemostasis as well as sufficient amounts of thrombin

Compensated but not optimal (susceptible to disruption in coagulation)

68
Q

What tests are valuable guides for patient with chronic liver disease to assess risk for bleeding?

A
  • TEG
  • ROTEM (rotational thromboelastometry)
69
Q

What causes baseline anemia in pts with CKD?

A
  • Lack EPO
  • Platelet dysfunction (d/t uremic environment)
70
Q

_________ and correction of anemia are both shown to shorted bleeding times

71
Q

What are treatments for platelet dysfunction associated with CKD?

A
  • Cryo
  • DDAVP
  • Conjugated estrogens given preop (x5 days)
72
Q

What is DIC?

A
  • Pathological hemostatic response to TF/7a complex causing excessive activation of the extrinsic pathway, which overwhelms the anticoagulant mechanisms and generates intravascular thrombin
  • Coagulation factors & platelets become depleted during widespread microvascular thrombotic activity, causing multi-organ dysfunction
73
Q

What may precipitate DIC?

A
  • Trauma
  • Amniotic fluid embolus
  • Malignancy
  • Sepsis
  • Incompatible blood transfusion
74
Q

What are lab findings indicative of DIC?

A
  • Low platelets
  • prolonged PT/PTT/thrombin time
  • increased soluble fibrin
  • fibrin degradation products
75
Q

What are primary actions in management of a pt in DIC/

A
  • Correct underlying condition
  • Administer appropriate blood products
76
Q

Uncontrolled _____________ is a common cause of trauma related death

A

hemorrhage

77
Q

What are common reasons for coagulopathies to occur in the trauma patient?

A
  • Acidosis
  • Hypothermia
  • Hemodilution
78
Q

What is Trauma induced coagulopathy (TIC)? What is thought to cause it?

A
  • Acute coagulopathy seen in trauma
  • Thought to be related to activated protein C decreasing thrombin thrombin generation
79
Q

What is the driving factor for protein C activation associated with trauma induced coagulopathy?

A
  • Hypoperfusion causing endothelial glycocalyx to degrade
  • proteoglycan-shedding results in “auto-heparinization”
  • platelet dysfunction contributes to the increased bleeding
80
Q

The most common inherited prothrombotic diseases are cause by a mutation in factor ______ or ______

A

V or Prothrombin

81
Q

What mutation leads to activated protein C resistance?

A

Factor V Leiden mutation
- present in 5% caucasion population

82
Q

What mutation causes increase prothrombin concentration leading to hypercoagulation?

A

Prothrombin mutation

83
Q

Inherited or acquired predisposition for thrombotic events:

A

Thrombophilia

84
Q

What is a typical presentation of thrombophilia?

A
  • Manifests as venous thrombosis
  • Highly susceptible to Virchows Triad (stasis, endothelial injury, hypercoagulability)
85
Q

Autoimmune disorder with antibodies against the phospholipid-binding proteins in the coagulation system:

A

Antiphospholipid Syndrome

86
Q

How is antiphospholipid syndrome characterized and what is often required?

A
  • Characterized by recurrent thrombosis and pregnancy loss
  • Often require life-long anticoagulants
87
Q

When is HIT likely to occur?

A

5-14 days after heparin treatment

88
Q

What is the MOA of HIT?

A

Autoimmune response occurring in up to 5% of pts receiving heparin

89
Q

What happens to platelets with HIT?

A

Platelet count reduction and activation of remaining platelets causing potential thrombosis

90
Q

If HIT is occurring: If a patient received a prior heparin dose __________ or __________ may occur with in 1 day of a subsequent dose

A

Thrombocytopenia
Thrombosis

91
Q

What are risk factors for development of HIT?

A
  • Women
  • Pt on high dose heparin (cardiopulm bypass)
  • unfractionated heparin carried higher risk than LMWH
92
Q

What are the step if HIT is suspected?

A
  • D/C all heparin
  • Convert to alternative AC (warfarin contraindicated because it decreases protein C and S synthesis)
93
Q

How is HIT diagnosis confirmed?

A

HIT antibody testing

antibodies typically cleared from circulation in 3 months

94
Q

How is Prothrombin time (PT) measured?

A

Plasma is mixed with TF and the number of seconds is measured until a clot forms

95
Q

What are PT measurements used to assess?

A
  • Assess integrity of extrinsic and common pathways
  • Used to monitor vitamin K antagonists s/a warfarin
96
Q

PT measurements can show deficiencies in which factors?

A

1, 2, 5, 7, 10

97
Q

What is activated partial thromboplastin time (aPTT) measuring?

A

Measures seconds until clot forms after mixing plasma w/ phospholipid, Ca, and an activator of the intrinsic pathway

98
Q

What are aPTT measurements used to assess?

A
  • Assess integrity of intrinsic and common pathways
  • May be used to measure the effect of heparin
99
Q

aPTT measurements are more sensitive to deficiencies in what factors?

100
Q

How is anti-factor Xa activity assay measured?

A

Plasma combined with Xa and an artificial substrate that releases a colorimetric signal after factor Xa is cleaved

101
Q

What are anti-factor Xa activity assays used to assess?

A
  • Functional assessment of heparin’s anticoagulant effect
  • Can also be used to assess effect of LMWH, fondaparinux, factor Xa inhibitors
102
Q

What is a normal platelet count?

A

> 100,000 plts/microliter
(POC testing is available)

103
Q

How is Activated Clotting Time (ACT) measured?

A

Variation of whole blood clotting time, with the addition of a clotting activator to accelerate clotting time

104
Q

What is ACT measurements used to assess?

A
  • Intrinsic and common pathway
  • Used to measure responsiveness to heparin
105
Q

What is a normal ACT?

A

107 +/- 13 seconds

106
Q

1 mg of protamine will inhibit ___ heparin

107
Q

What happens to heparin concentration if more protamine is added?

A

As increasing amounts of protamine are added to heparinized blood, time to clot decreases until protamine concentration > heparin concentration

108
Q

What is heparin concentration measurement used for?

A
  • Determines perioperative heparin concentration
  • Estimates plasma heparin concentration
109
Q

What does viscoelastic coagulation tests measure?

A

Measures all aspects clot formation from early fibrin generation to clot retraction and fibrinolysis - coagulation diagrams generated

110
Q

Why are viscoelastic coagulation test used? What are they?

A

Allows for more precise blood product administration
- TEG
- ROTEM (rotational thromboelastometry)

111
Q

What are the 3 main classes of antiplatelet agents?

A
  • Cyclooxygenase inhibitors
  • P2Y12 receptor antagonists
  • Platelet GIIb/IIIa R antagonists
112
Q

How do cyclooxygenase inhibitors work?

A

Block Cox1 from forming TxA2, which is important in platelet aggregation

113
Q

What are examples of COX inhibitors?

A
  • ASA: anti-platelets x 7-10 days after d/c
  • NSAIDs: anti-platelet effects x3 days
114
Q

How do P2Y12 receptor antagonists work?

A

Inhibit P2Y12-R→ preventing GIIb/IIIa expression

115
Q

What are some examples of P2Y12 antagonists?

A
  • Clopidogrel: anti-plt effects x7 days after d/c
  • Ticlopidine: anti-plt effects x14-21 days after d/c
  • Ticagrelor & Cangrelor: short acting, <24h activity
116
Q

How do Platelet GIIb/IIIa R antagonists work?

A

Prevent vWF & fibrinogen from binding to GIIb/IIIa-R

117
Q

What are examples of Platelet GIIb/IIIa R antagonists?

A
  • Abciximab
  • Eptifibatide
  • Tirofiban
118
Q

How do vitamin k antagonists work?

A

Inhibit synthesis of vit-k dependent factors 2, 7, 9, 10, protein C & S

119
Q

What is the most common vitamin k antagonist?

120
Q

Warfarin is the drug of choice for what?

A

Valvular Afib and valve replacements

121
Q

How long is the half life for warfarin?

A

40 hours - can take 3-4 days to reach therapeutic INR (2-3)
- Usually requires heparin until therapeutic effect achieved

122
Q

Considerations for patients on warfarin:

A
  • Need frequent lab monitoring required (PT/INR)
  • Reversable w/ vitamin K
123
Q

How does heparin work?

A

Binds to antithrombin→ directly inhibits soluble thrombin and Xa

124
Q

Unfractionated heparin:

A
  • Short half life, given IV
  • Fully reversable with protamine
  • Close monitoring required
125
Q

LMWH:

A
  • Longer half life than unfractionated
  • Dosed BID SQ
  • No coag testing needed
  • Protamine only partially effective
126
Q

Fondaparinux:

A
  • Much longer half life (17-21h), dosed once/day
  • Protamine not effective
127
Q

How do direct thrombin inhibitors work?

A

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

128
Q

What are examples of direct thrombin inhibitors?

A
  • Hirudin
  • Argatroban
  • Bivalirudin
  • Dabigatran (pradaxa)
129
Q

Where is hirudin naturally found?

130
Q

How is argatroban monitored?

A

Intraop with PTT or ACT

131
Q

Half life of argatroban:

A

45 minutes

132
Q

Which direct thrombin inhibitor has the shortest half life?

A

Bivalirudin

133
Q

What is bivalirudin the drug of choice for?

A

Renal or liver impairment

134
Q

What is the first direct oral anticoagulant?

A

Dabigatran (Pradaxa)

135
Q

What is dabigatran approved for?

A

CVA prevention and non-valvular a-fib

136
Q

What are the benefits to direct oral anticoagulants?

A
  • Have more predictable pharmacokinetics/dynamics
  • Fewer drug interactions
  • Dosed daily w/o lab monitoring
  • Efficacy similar to warfarin, but much shorter half-life
  • Fewer embolic events, intracranial hemorrhages, and lower mortality than warfarin
137
Q

What are examples of Direct Xa inhibitors?

A

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

138
Q

What are most thrombolytics?

A

Serine proteases that convert plasminogen to plasmin, which breaks down fibrinogen to fibrin

139
Q

What are the 2 categories of thrombolytics?

A
  • Fibrin-specific: Altepase (tPA), Tenecteplase
  • Non-fibrin-specific: Streptokinase (not widely used d/t allergic reaction)
140
Q

Surgery is contraindicated within ___ days of thrombolytic tx

141
Q

Absolute and relative contraindications for thrombolytics:

142
Q

What are procoagulants used for?

A

To mitigate blood loss

143
Q

What are the 2 classes of procoagulants?

A

Antifibrinolytics and factor replacements

144
Q

What are the 2 subclasses of antifibrinolytics?

A
  • Lysine analogues
  • SERPIN
145
Q

What do lysine analogues do?

What are the lysine analogues?

A

Bind and inhibit plasminogen from binding to fibrin and impairs fibrinolysis

  • Epsilon-amino-caprioc acid (EACA) & tranexamic acid (TXA)
146
Q

What is an example of a SERPIN?

A

Aprotinin (removed from market d/t renal & cardio toxicity)

147
Q

What are the factor replacements?

A
  • Recombinant VIIa
  • Prothrombin Complex Concentrate (PCC)
  • Fibrinogen concentrate
  • Cryoprecipitate and FFP
148
Q

What does recombinant VIIa do?

A

Increases thrombin generation via intrinsic and extrinsic pathways

149
Q

What does Prothrombin complex concentrate contain?

A

Contain vitamin-k factors

150
Q

One negative and positive of crycoprecipitate and FFP:

A
  • Cheaper and contain more coag factors
  • Less specific composition
151
Q

When to stop Warfarin prior to surgery:

A
  • Low rx pts should d/c 5 days prior to surgery & restart 12-24 hours postop
  • High rx pts should d/c 5 days prior & bridge w/ UFH or LMWH
152
Q

When to stop heparins prior to surgery:

A
  • UFH should be d/c’d 4-6h prior to surgery & resumed (no bolus) > 12h postop
  • LMWH should be d/c’d 24h prior to surgery & resumed 24h postop
153
Q

When to stop aspirin prior to surgery:

A

*not as defined
- Mod/high rx pts - current recommendation is to continue ASA
- Low rx pts - stop 7-10 days prior to surgery

154
Q

Preop guidelines for pts post coronary stent placement:

A
  • Bare-metal stents→ delay elective surgery 6 weeks after placement
  • Drug-eluding stents→ delay elective surgery 6 months after placement
155
Q

When might warfarin reversal be required?

A

For excessive bleeding or emergent surgery

156
Q

What is the drug of choice for emergent coumadin reversal?

A

Prothrombin complex concentrates

157
Q

What does vitamin k restore for reversal?

A

Vitamin K restores liver carboxylation of vit-k dependent factors for more sustained correction

158
Q

Is there a reversal for direct thrombin inhibitors?

A

No reversal for most, but half life is short

159
Q

What is the antidote for Dabigatran?

A

Idarucizumab

160
Q

What can direct factor Xa inhibitors be reversed by?

A

Andexanet - a derivative of factor Xa

161
Q

Common anticoagulants graph: