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2-Pharm Final > Anticoagulants > Flashcards

Anticoagulants Flashcards

1
Q

Define hemostasis.

A

to stop bleeding

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2
Q

What does hemostasis involve?

A

involves a complex inflammatory response that prevents exsanguination following injury, trauma, and/or surgery

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3
Q

When does hemostasis begin?

A

tissue injury & vascular endothelial disruption

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4
Q

What is the function of platelets?

A

work to form a primary plug to stop bleeding

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5
Q

Define adhesion.

A

involves GpIb attaching to vWF; makes platelets “sticky”

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6
Q

Define activation.

A

-involves tissue factor & platelets undergo conformational transformation; -GpIIb/IIIa receptor complexes on platelet surfaces enable platelets to link together to form a platelet plug

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7
Q

Define aggregation.

A

platelets release procoagulant mediators into the blood to form a primary unstable clot

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8
Q

Review the coagulation cascade.

A

Intrinsic, extrinsic, & common pathways

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9
Q

What is the current blood coagulation modeling involves in cell-based theory involving (2)?

A

Tissue Factor Pathway & Contact Pathway

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10
Q

Tissue Factor Pathway is the ______ Pathway)

A

Extrinsic

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11
Q

Contact Pathway is ______ Pathway

A

Intrinsic

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12
Q

Where does theorizes coagulation occur?

A

Theorizes coagulation occurs on different “cell surfaces” of platelets that bear Tissue Factor and these surfaces play a role in factor expression leading to hemostasis

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13
Q

What are the four phases of blood coagulation?

A

Initiation, amplification, propagation, & stabilization

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14
Q

Review the Blood Coagulation: Cell-Based Theory.

A
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15
Q

What is the initation phase of the Cell-Based Theory triggered by?

A

Triggered by injury to blood vessel endothelial surface

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16
Q

After injury, tissue factor recruits _____ & activates ________

A

Cell-Based Theory: Initiation Phase

  • recruits platelets & activates factor VII
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17
Q

What is the part of the Cell-Based Theory: Amplification?

A

As platelets mobilize to the site of injury, the amplification phase generates thrombin and additional clotting factors are activated

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18
Q

What factors does thrombin activates?

A

Cell-Based Theory: Amplification

  • Thrombin activates factors V, VIII, and IX
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19
Q

What does factor XI generate?

A

Cell-Based Theory: Amplification

  • Activated factor XI generates even more factor IX on the platelet surface
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20
Q

What does von willebrand factor promote?

A

Cell-Based Theory: Amplification

  • Von Willebrand factor promotes platelet aggregation through its adhesive properties w/GpIb and expression of GpIIb/IIIa causing additional platelet aggregation
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21
Q

What is the basis of Cell-Based Theory: Propagation?

A

All coagulation factors are actively influencing one another promoting coagulation

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22
Q

What does Activation of prothrombin results?

A

Cell-Based Theory: Propagation

  • in large burst of thrombin
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23
Q

What does thrombin convert?

A

Cell-Based Theory: Propagation

  • then converts fibrinogen to fibrin to form a stable secondary hemostatic plug
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24
Q

What does stabilization in the Cell based theory?

A

Cell-Based Theory: Stabilization

  • Stabilization results in fibrin (insoluble) clot formation
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25
Q

Review coagulation cascade.

A
  • Tissue Injury (Extrinsic Pathway)
  • Contact Activation (Intrinsic Pathway)
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26
Q

What is the physiologic balance of the coagulation system?

A

Delicate Physiologic Balance

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27
Q

Define Antithrombin.

A

Antithrombin (AT) - (previously known as AT III) is a member of the serine protease inhibitor family

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28
Q

What is the one of the most important natural proteins?

A

one of the most important natural proteins responsible for the prevention of spontaneous intravascular clot formation

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29
Q

What is the genetic components of Antithrombin definicency?

A

AT deficiency can be inherited or acquired

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30
Q

What is inherited AT deficiency?

A

inherited form is usually marked by extremely low levels of this endogenous anticoagulant

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31
Q

What does AT inhibit?

A

thrombin and also effectively inhibits factors XI, X, and IX

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32
Q

What are the characterisitics of congenital AT deficiency ?

A

Patients with congenital AT deficiency present with venous thromboses throughout life; develop many complications because of their hypercoagulable state and are unresponsive to heparin

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33
Q

How does heparin exert its effect?

A

Unfractionated heparin (UFH) exerts anticoagulant effect by binding to antithrombin (AT) in circulation

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34
Q

What does heparin binding to AT enhances?

A

the rate of thrombin-AT complex formation by 1000 to 10,000 times

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35
Q

What does heparin inhibit factors?

A

inhibits factors Xa & IIa

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36
Q

What does flood state about heparin?

A

Flood states other factors inhibited by AT: factors XII, XI, and IX

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37
Q

What does heparin inhibit?

A

factors Xa & IIa (factor IIa = thrombin)

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38
Q

What does anticoagulation of heparin depend on?

A

Anticoagulation depends on presence of adequate amounts of circulating AT

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39
Q

What is heparin pk?

A

Heparin is a highly charged acidic molecule administered IV or SC

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40
Q

Review anticoagulant pathways.

A
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41
Q

What is the aPTT of Heparin?

A

approx. 1.5 to 2.5 times normal values (typically 30-35 seconds)

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42
Q

What is the activated clotting time (ACT)?

A

used for high heparin doses (i.e., CPB); normal values 100-150 sec; in cardiac surgery, measured q30min – target 350-400sec

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43
Q

What is the anti-Xa assay of Heparin?

A

low-dose regimen: 0.3-0.5 units/mL, high-dose regimen: 0.5-0.8 units/mL

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44
Q

What is the clinical use of heparin?

A

prevention & tx of venous thrombosis, PE, acute coronary syndromes, perioperative anticoagulation for extracorporeal circulation & hemodialysis

45
Q

What is the main characteristics of Heparin-induced thrombocytopenia (HIT)?

A

Thrombocytopenia due to heparin injection/infusion can begin within hours of exposure

46
Q

When can severe thromobcytopenia from Heparin-induced thrombocytopenia (HIT) develop?

A

Severe thrombocytopenia can develop in some patients: 50% drop in platelet count/or <100,000 cells/µL

47
Q

What is Heparin-induced thrombocytopenia (HIT) caused by?

A

Caused by heparin-dependent antibodies to platelet factor IV that triggers platelet aggregation & thrombocytopenia

48
Q

What is HIT development?

A

heparin usually dc’d and patient switched to a different anticoagulant

49
Q

Heparin: _________ molecule

A

negatively-charged acidic

50
Q

Protamine: ___________ molecule

A

positively-charged alkaline

51
Q

What does protamine combine with heparin form?

A

form a stable complex devoid of anticoagulant activity

52
Q

How is the Protamine-heparin complex removed?

A

by the reticuloendothelial system (within tissues such as spleen, liver, lungs, bone marrow, & lymph nodes)

53
Q

What is the dose of protamine?

A

1mg for 100units of circulating heparin

54
Q

What are Low-Molecular-Weight Heparin?

A

Enoxaparin (Lovenox) & dalteparin (Fragmin) – administered via SC inj

55
Q

What are the LMWHs derived from?

A

from UFH and are depolymerized to yield fragments with a mean molecular weight 4,000 – 5,000 daltons

56
Q

LMWH anti-Xa to anti-IIa activity varies between _____ and _______.

A

4:1 and 2:1

57
Q

When is LMWH effects prlonged?

A

LMWH prolonged in patients with renal failure UFH should be used

58
Q

What is the delay of surgey for LMWH?

A

Surgery delayed 12 hrs after last dose of LMWH in patients w/normal renal function; longer w/renal dysfunction

59
Q

What is a risk with LMWH?

A

Risk of epidural/spinal hematoma

60
Q

What does protamine not reverse?

A

LMWH anticoagulation

61
Q

What is the characteristics of Fondaparinux (Arista)?

A

Synthetic anticoagulant resembles active sites of a heparin molecule that binds AT

62
Q

What does Fondaparinux (Arista) inhibit?

A

inhibits factor Xa but not thrombin

63
Q

What is Fondaparinux (Arista) used for?

A

Used for DVT prophylaxis, patients w/PE, & alternative anticoagulant in patients with HIT

64
Q

How are Fondaparinux (Arista) used?

A

Administered SC inj

65
Q

What is the duration of action/elimination half time of Fondaparinux (Arista)?

A

Long duration of action/elimination half-time = 15 hours

66
Q

When is Fondaparinux (Arista) not used?

A

Not used in patients w/renal failure (primarily renally excreted)

67
Q

What is an example of Direct Thrombin Inhibitors?

A

Bivalirudin & Argatroban

68
Q

What is the MOA Direct Thrombin Inhibitors: Bivalirudin?

A

Binds directly to factor IIa – thrombin

69
Q

When is Direct Thrombin Inhibitors: Bivalirudin indicated?

A

Indicated for patients w/ unstable angina undergoing PTCA or patients w/ HIT

70
Q

What is the MOA of Direct Thrombin Inhibitors: Argatroban?

A

An injectable, synthetic univalent direct thrombin inhibitor

71
Q

What is the indication for Direct Thrombin Inhibitors: Argatroban?

A

Indicated for prophylaxis or tx of thrombosis in patients with or at risk for HIT and undergoing PCI

72
Q

What is the elimination of Direct Thrombin Inhibitors: Argatroban?

A

Hepatic elimination

73
Q

What is the dose adjustment Direct Thrombin Inhibitors: Argatroban in renal dysfunction?

A

no dose adjustment required in patients w/renal dysfunction

74
Q

What is an example of a Vitamin K Antagonist?

75
Q

What is the formularities of Vitamin K Antagonist: Warfarin?

A

Oral anticoagulant

76
Q

What is the characterisitics of Vitamin K Antagonist: Warfarin?

A

Most frequently used oral anticoagulant b/c predictable onset & duration of action, excellent bioavailability after oral administration

77
Q

What is the MOA of Vitamin K Antagonist: Warfarin?

A

inhibits vitamin K synthesis and thereby inhibiting production of vitamin K-dependent clotting factors II, VII, IX, & X

78
Q

What is the bioavailability of Vitamin K Antagonist: Warfarin?

A

Oral bioavailability of 100%

79
Q

What is the protein binding of Vitamin K Antagonist: Warfarin?

A

97% protein-bound to albumin (this means is easily displaced by other highly protein-bound drugs)

80
Q

What is the onset of action of Vitamin K Antagonist: Warfarin?

A

delayed onset of action (8-12 hours)

81
Q

What is the peak effect of peak effect of Vitamin K Antagonist: Warfarin?

A

peak effects do not occur for 36-72 hours

82
Q

What is the metabolism of Vitamin K Antagonist: Warfarin?

A

hepatic metabolism

83
Q

What is the clinical use of Vitamin K Antagonist: Warfarin?

A

VTE prophylaxis, prevention of systemic embolization/stroke in patients w/Afib or prosthetic heart valves, patients w/hypercoagulable states

84
Q

What is the lab evaluation of Vitamin K Antagonist: Warfarin?

A

tx guided by measurement of PT

85
Q

What is the standardized system of measurement of Vitamin K Antagonist: Warfarin?

A

INR measurement overcomes variability of PT measurement among various labs – is a standardized system of measurement

86
Q

What is the target INR for Vitamin K Antagonist: Warfarin?

A

target INR 2.0-3.0 for patients requiring moderate anticoagulation (prosthetic heart valves)

87
Q

What does unexpected fluctuations in dose response to warfarin may reflect?

A

changes in diet, undisclosed drug use, poor patient compliance, patient self-medication, alcohol consumption

88
Q

What can affect warfarin?

A

Concomitant OTC & prescription drugs can augment or inhibit the anticoagulant effect of warfarin

89
Q

What can potentiate warfarin’s anticoagulation effects?

A

can be potentiated in patients w/inadequate vitamin K intake, preexisting liver disease, & advanced age

90
Q

Patients receiving warfarin should have ______ checked preop

91
Q

What is the recommendation of minor surgery procedures with anticoagulants?

A

can be safely performed in pts receiving oral anticoagulation

92
Q

What is the recommendation of major surgery procedures with anticoagulants?

A

recommended to DC 1-3 days preop to enable PT to return to within 20% of normal range

93
Q

When should anticoagulation be reinstituted?

A

reinstitution of oral anticoagulation 1-7 days postop

94
Q

High-risk patients (pts w/prosthetic heart valves) may require bridging with ___

95
Q

_______ is the main complication of anticoagulation

A

Bleeding (esp. w/concomitant use of aspirin)

96
Q

What can anticoagulation drugs increase the incidence of?

A

Anticoagulation drugs may increase incidence of intracranial hemorrhage after CVA

97
Q

What is the Warfarin reversal?

A

Vitamin K IV or PO can be used; will not immediately reverse anticoagulant effect

98
Q

What can be given for immediate Warfarin reversal?

A

(i.e., performance of high-risk surg procedures such as craniotomy): prothrombin complex concentrates (PCCs) or FFP

99
Q

What is the components of Rivaroxaban (Xarelto) ?

A

Oral, direct factor Xa inhibitor

100
Q

What does Rivaroxaban (Xarelto) not require?

A

Doesn’t require AT as a cofactor

101
Q

What molecule is Rivaroxaban (Xarelto)? What could it potentially treat?

A

Is a non-heparin like molecule; may be suitable for mgmt. of patients w/HIT

102
Q

When is Rivaroxaban (Xarelto) used?

A

Used in HIT patients, DVT prophylaxis, patients w/Afib, treatment of DVT/PE, in combo w/ASA to reduce risk of major CV events in patients w/chronic CAD or peripheral artery dz

103
Q

What is the relationship of Rivaroxaban (Xarelto) and neuraxial anesthesia?

A

risk of epidural hematoma; follow ASRA guidelines in patients taking rivaroxaban & epidural catheter management

104
Q

What is the formulary for Apixaban (Eliquis)?

A

Oral, direct factor Xa inhibitor

105
Q

What is the use for Apixaban (Eliquis)?

A
  • Approved to reduce risk of stroke & systemic embolism in patients w/Afib
  • DVT prophylaxis; patients having hip or knee replacement surgery
  • tx of DVT/PE & reduce risk of recurrent DVT/PE
106
Q

What is the relationship of Apixaban (Eliquis) and neuraxial anesthesia?

A

risk of epidural hematoma; follow ASRA guidelines in patients taking rivaroxaban for epidural catheter management

107
Q

What is the MOA of Dabigatran (Pradaxa)?

A

Oral, direct thrombin inhibitor

108
Q

What is the Dabigatran (Pradaxa) used for?

A
  • approved to reduce risk of stroke & systemic embolism in patients w/Afib
  • tx of DVT/PE & reduce recurrence of DVT/PE
109
Q

What labs are important with Dabigatran (Pradaxa)?

A

Anticoagulant effects measured by thrombin time, clotting time; can use activated PTT for screening

2-Pharm Final (10 decks)

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