Anticoagulants Flashcards

1
Q

Anticoagulants alters?

A

Alters coagulations cascade

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2
Q

Antiplatelets prevent ________by _______

A

Prevent formation of clot by blocking platelets

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3
Q

Fibrinolytics

A

Work in fibrinolytics pathway, BREAK DOWN CLOTS

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4
Q

**Prothrombin: In particular, this test measures the activity of 3 specific vitamin K dependent clotting factors

A

Factors II, VII, X

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5
Q

*****Prothrombin (PT)

Which pathway?

A

Determines the function of the extrinsic system and the

common pathway of the coagulation system

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6
Q

activated PTT is

Which pathway?

A

Measures the activity of the intrinsic and common pathway of the coagulation system

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7
Q

INR

A

Mathematical correction of prothrombin time

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8
Q

aPTT used for what 2 main medications class

A

The aPTT is widely used for monitoring unfractionated heparin and INJECTABLE direct thrombin inhibitors

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9
Q

aPTT Measures factors:

A

IXa, Xa, and XIIa

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10
Q

aPTT not used for those patients ? used ?

A

Lupus Anticoagulant (LAC); ACT

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11
Q

What does ACT measure?

A

• Measures the activity of the intrinsic and common pathway of the coagulation system

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12
Q

What is the normal ACT range?

A

100-150

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13
Q

Used to manage (ACT Test)

A

Cardiothoracic surgery

PCI

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14
Q

What is the goal of ACT for most procedures

A

300-450 seconds

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15
Q

Thrombin Time monitors _____and normal is ____

A

Factor IIa; <30seconds

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16
Q

If Thrombin time is prolonged, 2 reasons:

A
  • deficiency of fibrinogen

- inhibition of thrombin

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17
Q

Any drugs that decreases thrombin activity would elevated:–>

A

Thrombin Time

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18
Q

Anticoagulants and Spinal/Epidural HEMATOMA WARNING

A

DO a risk assessment before for patients on unfractionated heparin, fonduparix
Use of indwelling epidural catheters
• Concomitant use of other drugs that affect hemostasis, NSAID’s, platelet inhibitors or other anticoagulants
• A history of traumatic or repeated epidural or spinal punctures
• A history of spinal deformity or spinal surgery

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19
Q

Unfractionated heparin derived from?

A

Derived from PIG INTESTINE mucosa

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20
Q

Unfractionated heparin MOA

A

Heparin acts by FIRST binding to and forming a complex with antithrombin (formally called antithrombin III, AT-III) causing a conformational change in AT which accelerates the action of antithrombin (endogenous coagulants) by 1,000 fold or more.
**The AT/Heparin complex then irreversibly inhibits the activated coagulation factors IIa, IXa, Xa, XIa and XIIa

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21
Q

The AT/Heparin complex

A

inhibits the activated coagulation factors IIa, IXa, Xa, XIa and XIIa

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22
Q

_______is a required cofactor for UFH anticoagulant effects

A

Antithrombin

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23
Q

• By inactivating thrombin (factor IIa), heparin not only prevents fibrin formation but also

A

inhibits thrombin-induced activation of factor V and factor VIII

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24
Q

2 main ones carrying the action of heparin

Most sensitive by the AT/Heparin complex

A

Thrombin (IIa)

Factor Xa

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25
Q

Heparin must bind to BOTH________And ________ to form a Ternary Heparin/AT/Thrombin Complex in order for thrombin to be

A

AT and thrombin; inactivated

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26
Q

Heparin need __________ via its high-affinity pentasaccharide sequence in order to ______

A

only bind to AT

to inactivate factor Xa

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27
Q

Heparin blocks the

A

intrinsic and common pathways of the coagulation cascade

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28
Q

Heparin display what kind of pharmacokinetics

A

nonlinear pharmacokinetics, half life useless

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29
Q

Heparin cross lipid barriers?

Lipid soluble?

A

Heparin is a poorly lipid-soluble, high-molecular weight substance that cannot cross lipid barriers in significant amounts

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30
Q

2 routes for heparin

A

SC and IV

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31
Q

• NEVER give UFH via_______ due to potential for large

hematoma formation

A

IM route

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32
Q

____ and_______can prolong the biologic t1/2 of heparin

A

Hepatic disease and renal dysfunction

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33
Q

Heparin effects will

A

vary amont patient to patient

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34
Q

Clearance mechanism of Heparin

2 mechanisms:

A
  • First, heparin is cleared and degraded primarily by th RETICULOENDOTHELIAL system, this is a rapid and saturable process (that’s why its NONLINEAR)
  • At therapeutic doses, a large proportion of heparin is cleared through this mechanism

• A second slow and non-saturable process involves renal clearance of undergraded heparin and this predominates at very higher doses

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35
Q

Does heparin cross placenta?

drug of choice for pregnant patient

A

NO; heparin

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36
Q

The anticoagulant activity of heparin can be monitored using any of the following tests:

A
  1. aPTT (activated Partial Thromboplastin Time)
  2. ACT (Activated Clotting Time)
  3. Heparin anti-factor Xa assay
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37
Q

Heparin Anticoagulants monitoring:
monitors?
sensitive to which factors?
APTT ration of ____to _____the control reagent/normal value is the goal for coagulation

A

aPTT (activated Partial Thromboplastin Time)
• Sensitive to levels of thrombin (IIa), factor IXa, Xa and XIIa
aPTT ratio of 1.5 to 2.5 times the control reagent/normal values is the goal for anticoagulation

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38
Q

aPTT assess 2 pathways

A

Intrinsic and final common pathways

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39
Q

Used to monitor higher heparin doses and concentrations given to patients undergoing _____or ______ procedures

A

PCI and CABG

ACT (300-450 seconds maintained throughout entire procedures)

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40
Q

This is the most accurate assay for monitoring UFH therapy (outside of OR)
Expected therapeutic range is

A

Heparin anti-factor Xa assay

0.3-0.7 anti-Xa units/mL

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41
Q

VTE Prophylaxis

A

• Heparin 5000 units SQ q 8 - 12 hours

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42
Q

Coagulation of heparin is based on (dosing)

A

WEIGHT

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43
Q

• Heparin requirements are increased during

A

pulmonary embolic disease

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44
Q

• Heparin requirements are reduced and elimination t1/2 is prolonged in

A

hypothermia

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45
Q

Nitroglycerin has been reported to ________heparin’s

anticoagulant effects which may the required dose of heparin

A

decrease; increase

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46
Q

Most common site of bleeding for Heparin is the

A

GI tract

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47
Q

Anaphylactoid and hypersensitivity reactions

A

Fever, chills, urticaria, tachycardia, hypertension, dyspnea, cardiopulmonary arrest

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48
Q

Heparin is protein bound

A

YEs highly,

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49
Q

Heparin can displace those drugs

A

Diazepam and propranolol

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50
Q

• Thrombocytopenia resulting from the use of heparin products can be classified into two distinct categories/syndromes

A
  • Heparin-associated thrombocytopenia (HAT)- harmless

* Heparin-induced thrombocytopenia (HIT)

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51
Q

Thrombocytopenia defined as

platelet range for thrombocytopenia

A

Early, mild, transient fall in platelet count

Defined as a platelet count of 100 – 130 × 103/mm3

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52
Q

Thrombocytopenia occurs when?

What percentage of patients

A

Occurs 1 – 4 days after the start of heparin therapy

25%

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53
Q

Body from antibodies

A

IgG

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54
Q

Pathophysiology of Thrombocytopenia

A
  • PF4 found on endothelial cells and platelets
  • Heparin binds to PF4 forming a heparin-PF4 complex. IgG antibodies in circulation bind to this complex & activate platelets & cause the release of prothrombotic
    microparticles, platelet consumption, thrombocytopenia & thrombosis
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55
Q

Diagnosis of HIT is based on both clinical and serological findings:
Platelet count
onset within ________days

A
  • Platelet count drop < 150,000 mm3 OR 50% drop in baseline platelet count (even if the platelet count is > 150,000 mm3)
  • Onset within 5-14 days after starting ANY UFH product
  • Thrombosis associated with thrombocytopenia
  • Other causes of thrombocytopenia ruled out
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56
Q

**To have a diagnosis of HIT you must have the presence of_____________

A

Anti-PF4-Antibodies

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57
Q

Treatment of HIT

A
  • remove intra-___catheter

- Used an INJECTABLE Direct thrombin inhibitors.

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58
Q

Reversal Agent of heparin

A

• Protamine sulfate is the antidote to the anticoagulation effect from unfractionated heparin therapy

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59
Q

Action of protamine (acid base reaction)

A

Protamine is a POSITVELY charged strong base polypeptide that interacts with NEGATIVELY charged acidic heparin molecules via a neutralization reaction (acid-base interaction) to form a STABLE SALT COMPLEX that has no anticoagulant properties.
These heparin-protamine complexes are then removed by the RETICULOENDOTHELIAL system

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60
Q

Protamine Reversal Dosing

Dose is _______protamine to inactive ______Units of heparin

A

• Dose is approximately 1 mg of protamine to inactivate 100 USP units of heparin predicted to still be in circulation

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61
Q

• Another calculation used is administration of ______of protamine for each 100 USP units of heparin present as calculated from the ACT

A

1.3 mg/kg

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62
Q

• Clearance of protamine by the reticuloendothelial system (within_______) is more rapid than heparin clearance and this may explain, in part, the phenomenon of heparin rebound

A

20 minutes)

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63
Q

*****• Dose is approximately 1 mg of protamine to inactivate

A

100 USP units of heparin PREDICTED TO STILL BE IN CIRCULATION

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64
Q

To predict how much heparin useful to know

A

last infusion rate, last 2 hours

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65
Q

Protamine sulfate’s t1/2 =

A

7 minutes (short)

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66
Q

Protamine Adverse effects

A

Hypotension
*Bradycardia
**
Dyspnea
**
Flushing feeling of warmth
Acute pulmonary hypertension
Edema
Bronchoconstriction
RVF

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67
Q

Rapid IV injection of protamine may be associated with

A
Histamine release causing :
severe hypotension
bradycardia
facial flushing 
dyspnea.
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68
Q

Rapid IV also can lead to

A

increase the risk of anaphylactoid reactions

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69
Q

Max infusion rate of Protamine

A

5mg/min

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70
Q

Allergic reactions to protamine have been described most often in_________ preparations containing protamine

A

diabetics receiving insulin

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71
Q

• Patients that are _____ _______may have a higher incidence of allergic reactions to protamine since protamine sulfate is derived from fish sperm

A

allergic to fish

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72
Q

• LMWHs are NEVER

A

clinically interchangeable with one another on a unit-for-unit basis! because of the molecular size and action

73
Q

3 low molecular weights heparin are (-parin)

A
  • Lovenox® (Enoxaparin)
  • Fragmin® (Dalteparin)
  • Innohep® (Tinzaparin)
74
Q

Low Molecular Weight Heparins:

Mechanism of Action

A

• LMWH’s first bind to antithrombin by a unique pentasaccharide sequence —->a conformational change in antithrombin and this LMWH/AT complex then inactivates factor Xa and inactivates to a lesser degree thrombin (factor IIa), BUT both factors are inactivated

75
Q

LMWH inactivates those two factors

A

Xa (more) and IIa (less)

76
Q

why LMWH inactivates Xa more because

A

more selective because they are two short to form the complex

77
Q

Heparin vs. LMWH
Produces a more______and______duration of
anticoagulant response compared to UFH since LMWH’s have less_________ to circulating and cellular proteins compared to UFH

A

PREDICTABLE & longer ;binding

78
Q

LMWH • t1/2 is dose_______and prolonged in _________

A

-INDEPENDENT and prolonged in renal dysfunction

79
Q

LMWH Excretion

• Cleared primarily via the

A

kidneys

80
Q

Pharmacokinetics of low molecular weight heparin, they do follow linear pharmacokinetics so wait at least ________steady state

A

4-5

81
Q

• Routine anticoagulant laboratory monitoring for LMWH (necessary/not necessary) due to their predictable anticoagulant response and pharmacokinetic profile

A

IS NOT necessary

82
Q

***_________level for LMWH is the recommended test if

anticoagulant monitoring is required

A

• Antifactor-Xa

83
Q

For LMWH, you must monitor which organ?

A

renal function

84
Q

Adverse effects of LMWH

A

Bleeding

85
Q

NO antidote for LMWH but on a test_____________ is the antidote, % of neutralization

A

Protamine, neutralization up to 60%

86
Q

****Low Molecular Weight Heparins:

Neuraxial Anesthesia Implications

A

Spinal anesthesia/epidural anesthesia/LP
• Prior to procedure, wait at least 12 hours (once daily prophylaxis doses) or 24 hours (BID prophylaxis or treatment doses) after the last dose of LMWH BEFORE CONsidERING catheter placement

87
Q

**Administer first dose of LMWH a MINIMUM of

A

2 hours AFTER the catheter has been removed

88
Q

AriXtra® (fondaparinux)

A

synthetic pentasaccharide class agent

89
Q

Is AriXtra heparin?

A

Is a Non-Heparin Product!

90
Q

How does ariXtra acts? selective, (direct/indirect)

A

• Is a selective, in-direct inhibitor of Factor Xa only!

91
Q

Which factor does ARIXTRA inhibit?

A

Factor Xa

92
Q

What does ARIXTRA does NOT DO?

A

DOES NOT increase the rate of thrombin inhibition

by antithrombin

93
Q

AriXtra indirectly inhibits ONLY factor Xa by

A

reversibly binding to antithrombin

94
Q

AriXtra half life is

A

long

95
Q

Main route of elimination for AriXtra

A

Kidneys

96
Q

Does Arixtra cause HIT?

A

No

97
Q

There is______reversal agent for fondaparinux (ariXtra)

A

NO

98
Q

Most serious complication of AriXtra

A

Bleeding

99
Q

Direct Thrombin Inhibitors

Mechanism of action

A

• Direct thrombin inhibitors bind DIRECTLY to thrombin (factor IIa) and inhibit thrombin’s functions/actions

100
Q

**Direct Thrombin inhibitors Inhibits both ____and ________

A

BOTH free and clot-bound thrombin (factor IIa)

101
Q

Direct thrombin inhibitors do not bind to plasma protein and are

A

• Are AT-Independent (These agents do not require

antithrombin as a cofactor for their anticoagulant response)

102
Q

Is there an antidote for PARENTERAL direct thrombin inhibitors?

A

There is currently no antidote available for any

PARENTERAL direct thrombin inhibitor agent!

103
Q
  • Direct thrombin inhibitors increase/prolong all of the following anticoagulation laboratory tests: most used ?
  • aPTT, thrombin time, PT/INR, chromogenic anti-IIa assays, and the ecarin clotting time
A

ACT,

104
Q

4 direct PARENTERAL Direct thrombin inhibitors

A
  1. Angiomax (bivalirudin)
  2. Argatroban

IPRIVASK (desirudin)
REFLUDAN

105
Q

Iprivask® (Desirudin)

A

Binds irreversibly, selectively & directly to inhibit both clot-bound and free thrombin (Factor IIa)

106
Q

Only monitoring for Desirudin

A

aPTT

107
Q

• Desirudin is an _______inhibitor!

A

irreversible

108
Q

Stop time of desirudin prior to surgery

A

24 hours

109
Q

Lepirudin

Removed from market for FINANCIAL issue

A

a 1:1 stoichiometric complex with thrombin and causes irreversible inhibition of thrombin

110
Q

Lepirudin is a derivative of

A

derivative of hirudin

111
Q

Lepirudin used for patients with ______

A

USed for HIT patients

112
Q

Direct Thrombin Inhibitors:

Angiomax® (Bivalirudin) Mechanism of action

A

Mechanism of action
• Reversibly binds directly to clot-bound and free thrombin and inhibits thrombin and thus inhibits fibrin formation
- Reversibility means thrombin itself can cleave bivalirudin from the active site after bivalirudin has bound to it and thrombin can resume its hemostatic function

113
Q

Elimination of angiomax 2 ways?

A

Elimination

• Kidneys (20%) & Enzymatic metabolism (80%)

114
Q

Laboratory monitoring of anticoagulant effects (depends on indication) for angiomax
• HIT________
• PCI or CABG use __________

A

use aPTT: Goal 1.5–2.5x control

ACT: Goal 300–450 seconds

115
Q

Angiomax SToP time prior to surgery

A

4-6 hours

116
Q

To know if effect of Bivalirudin are gone, because those labs correlate very well with those drugs.

A

ACT or aPTT

117
Q

**Angiomax® (Bivalirudin)

• Clinical uses

A

Used as an alternative to heparin in patients undergoing

cardiopulmonary bypass surgery

118
Q

Argatroban is a _________inhibitor derived from the amino acid _________

A

inhibitor derived from L-arginine

119
Q

Argatroban Mechanism of action

A

Competitive inhibitor of thrombin that binds reversibly to the active site of both clot-bound and free thrombin and inhibits thrombins function and thus inhibits fibrin formation
• Reversibility means thrombin can cleave argatroban from the active site after argatroban has bound to it and thrombin can resume its hemostatic function

120
Q

Clinical uses ARGATROBAN

A

Is an alternative to heparin for anticoagulation in patients requiring CABG, especially in the presence of HIT

121
Q

Direct Thrombin Inhibitors:

Argatroban Metabolism

A

Hepatic

122
Q

Dialysis /RENAL Dysfunction patients may use

A

Argatroban

123
Q

Laboratory monitoring of anticoagulant effects (depends on indication) for ARGATROBAN
• HIT________
• PCI or CABG use __________

A

use aPTT: Goal 1.5–2.5x control

ACT: Goal 300–450 seconds

124
Q

Oral Direct Thrombin Inhibitor

A

Pradaxa (dabigatran)

125
Q

Pradaxa (selective, reversible, competitive)

A

Is a synthetic, selective, reversible, competitive direct thrombin inhibitor that is only given ORALLY

126
Q

Pradaxa® (dabigatran) is _______and requires conversion into its pharmacologically active form

A

prodrug

127
Q

After oral administration, dabigatran etexilate is metabolized by

A

esterase enzymes into the active form dabigatran

128
Q

• Dabigatran (the active form) is then further metabolized in the liver by

A

non-CYP 450 pathways forming several glucuronide active metabolites that have similar pharmacological activity to dabigatran

129
Q

Pharmacokinetics of dabigatran

hafl life/Clearance via?

A

long half life

Clearance kidneys

130
Q

__________monitoring is required to assess the anticoagulant effect since dabigatran exhibits a predictable pharmacokinetic and pharmacodynamic profile

A

No routine coagulation

131
Q

if patient is on pradaxa, check those 2 labs before spinal anesthesia, if elevated do not administer spinal anesthesia

A

Thrombin time

Ecarin clotting time

132
Q

Adverse effects of PRADAXA

A

Dyspepsia

Bleeding

133
Q

Pradaxa® (Dabigatran etexilate):
Neuraxial Anesthesia Implications
• Spinal anesthesia/epidural anesthesia/LP
Prior to procedure wait a minumum of _______

A

Pradaxa® is not recommended in patients undergoing anesthesia with post-operative indwelling epidural catheters in place
• Prior to procedure, wait a minimum of 72 hours or longer in renal failure BEFORE catheter placement
• Administer first dose of Pradaxa® a MINIMUM of 2 hours after the catheter has been removed

134
Q

Idarucizumab (Praxbind)

A

monoclonal antibody fragment

135
Q

Antidote of PRADAXA

A

Idarucizumab (Praxbind)

136
Q

Mechanism of action of Idarucizumab?

A

• Idarucizumab binds directly to dabigatran and its metabolites with higher affinity than the binding of dabigatran to thrombin and neutralizes their anticoagulant effect immediately after administration

137
Q

3 Oral Direct Factor Xa Inhibitors: (-xaban)

A

Rivaroxaban (Xarelto®)
• Apixaban (Eliquis®)
• Edoxaban (Savaysa®)

138
Q

Oral Direct Factor Xa Inhibitors: (-xaban) Mechanism of action

A

These agents bind to and inhibit both free factor Xa, clot-bound factor Xa, and factor Xa within the prothrombinase complex and thus inhibit thrombin (factor IIa) generation indirectly via inhibition of factor Xa

139
Q

For oral direct factor Xa inhibitors, anticoagulation effects usually take how long ?

A

anticoagulant effects usually within 1-3 hours depending on the agent

140
Q

Rivaroxaban , Apixaban and Edoxaban MOA and excretion

A

Direct Factor Xa Inhibitors

Kidney and feces

141
Q

_____________is the most useful test to check the anticoagulant effect of rivaroxaban or apixaban

A

A chromogenic anti-Xa assay

142
Q

Monitor for Oral direct factor Xa

A

bleeding

143
Q

Rivaraxaban and Apixaban antidotes

A

ANDEXXA

144
Q

ANDEXXA adverse reaction

A

UTI, Pneumonia

145
Q

Rivaroxaban, Apixaban, Edoxaban:
Neuraxial Anesthesia Implications
• CONTRAINDICATED to use_____________
• Concomitant use of antiplatelet agents (ASA, clopidogrel, etc.), NSAIDs or any other medication that also causes bleeding withrivaroxaban, apixaban, or edoxaban further increases the patients risk of bleeding

A

FULL anticoagulant doses of these agents while spinal catheter is in place

146
Q

Coumadin® (Warfarin):

Mechanism of Action

A

Warfarin acts by inhibiting the enzyme vitamin K epoxide
reductase (VKOR). Inhibiting this enzyme prevents the
conversion of oxidized vitamin K epoxide into its reduced form and this prevents the SYNTHESIS of the vitamin K-dependent clotting factors II (prothrombin), VII, IX, X

147
Q

is the only vitamin K antagonist agent available for

clinical use

A

• Warfarin

148
Q

Warfarin does not attach to

What does it inhibit?

A

Any factors

inhibit enzymes responsible to make those factors

149
Q

Affects liver’s abiltiy to synthesize

A

protein C and protein S

150
Q

Warfarin is available as a racemic mixture of R and S isomers both
• Warfarin interferes with the

A

active

extrinsic pathway

151
Q

Warfarin pharmacokinetics absorption

A

Rapid and completely absorbed

152
Q

Warfarin Protein binding:

A

97% protein bound to albumin

153
Q

Metabolism of warfarin:

A

Metabolized in the liver via multiple CYP 450 enzymes into inactive metabolites, which are excreted in both the bile and urine

154
Q

Enhanced anticoagulant effect of warfarin in the presence of _____disease

A

liver

155
Q

The elimination of warfarin is almost entirely by _______

A

Metabolism

156
Q

Warfarin half life ranges between

A

20 – 60 hours

157
Q

Warfarin acts by inhibiting the enzyme

A

vitamin K epoxide reductase (VKOR).

158
Q

Pharmacodynamics of warfarin

The time to onset and offset of the anticoagulant effect of warfarin is delayed by 2 main factors:

A
  1. The long elimination half-life of warfarin (20 – 60 hours)
  2. The elimination half-life of the already made 4 vitamin Kdependent clotting factors
159
Q
  • ***Onset of effect of warfarin: within_____ hours (due to___ depletion)
  • ***Full effect:______ (due to Factor____ depletion)
A

24; Factor VII

5-7 days; Factor II

160
Q

Coumadin® (Warfarin):
Reversal Agents
Anticoagulant effects are reversed by administering: (5)

A
  1. Vitamin K (IV or PO)
  2. FFP
  3. Prothrombin Complex Concentrates(PCC)
  4. Activate prothrombin Complex concentrates
  5. Recombinanct factor VIIa (last resort)
161
Q

• Do not administer vitamin K

A

SQ or IM

162
Q

• Vitamin K IV can cause ________ reactions – mix in a minimum of __________and infuse over a minimum of to minimize this from occurring

A

anaphylactic reactions ; 50 ml of IV fluid; 20 minutes

163
Q

______ Is the first FDA-Approved 4-Factor Prothrombin Complex Concentrate (PCC) for warfarin reversal in the United States

A

Prothrombin Complex Concentrate (Human),

Kcentra

164
Q

Warfarin tells body to stop ______(making those factors)

A

Factor II, VII, IX and X

165
Q

• Mechanism of action of Kcentra
Contains factors ___ ___ ____ ___ and _______ and ____
This product rapidly ________________ as well as ____________ (these factors are_____by warfarin)

A

“Just giving what warfarin prevented the body from making”
• Kcentra® contains factors II (prothrombin), VII, IX and X, and antithrombotic proteins C and S
• This product rapidly increases plasma levels of the vitamin K- dependent coagulation factors II, VII, IX, and X as well as the antithrombotic proteins C and S (these are all factors that are reduced by warfarin)

166
Q

KCentra is only given via which route?

A

IV

167
Q

• Warfarin + CYP 450 inhibitor

A
  • Increases warfarin plasma levels & increase risk of bleeding
  • i.e.: Amiodarone, quinidine
168
Q

INR >2

A

cannot do spinal anesthesia

169
Q

• Warfarin + CYP 450 inducer

A
  • Decreases warfarin plasma levels & decreases risk of bleeding & increases risk of possible thrombotic complications
  • i.e.: Rifampin, phenytoin, barbiturates, carbamazepine
170
Q

Goal INR therapy is

A

2-3

171
Q

Warfarin Anticoagulant effects are monitored using the

A

prothrombin time/international normalized ratio (INR) test

172
Q

• The higher the INR,

A

the greater the risk of bleeding

173
Q

Can warfarin cross placenta

A

yes

174
Q

Surgical and Spinal Anesthesia Implications
• Spinal anesthesia/epidural anesthesia/LP
** Hold Time Before Epidural Placement:_______

A

*****4-5 days & INR < 1.5

175
Q

Contraindicated while catheter is in place

• Hold Time After Epidural Removal:_______

A

2 hours

176
Q

• Urgent reversal of warfarin prior to surgery – administer

A

Vitamin K IV via slow infusion or can give FFP or Kcentra®

177
Q

Assess for bleeding risks:

A

thrombotic risks and the type of surgical procedure.

178
Q

Pradaxa, to know is not present, what test?

A

Ecarin Clotting time (ECT) and thrombin time (TT)