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Antithrombotics Flashcards

1
Q

What is the action of anticoagulants?

A

Prevents clot formation & extension (doesn’t help against pre-existing clots)

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2
Q

What is the action of fibrinolytics?

A

Breaks up existing clots

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3
Q

What is the action of antiplatelets?

A

Interferes with platelet activity

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4
Q

What are the 2 types of thrombi?

A

White thrombus

Red thrombus

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5
Q 
Describe the makeup of white thrombi and where they form.
Which medication class would be most effective?
A
  • Platelet rich
  • Forms in the arteries i.e. coronary artery clot
  • Antiplatelets: good for s/p M.I for 2nd prevention
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6
Q 
Describe the makeup of red thrombi and where they form.
Which medication class would be most effective?
A
  • Fibrin and RBC-rich
  • Forms in the veins i.e. DVT, P.E.
  • Anticoagulants
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7
Q

What are some common sites for DVTs? Complication? White clot or red clot?

A
  • Iliac vein, femoral vein, popliteal vein, small saphenous vein
  • Proximal leg veins more likely to become P.E
  • Fibrin-rich red clot
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8
Q

Is a P.E. thrombus likely a white or red clot?

A

Red clot

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9
Q

Is a CVA more likely a white or red clot?

A

White clot

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10
Q

Is an acute myocardial infarction mor4e likely a white or red clot?

A

White clot

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11
Q

What is the action of thromboxane A2 (TXA2)?

A
  • Vasoconstriction

- Platelet activation

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12
Q

What does vonWillebrand Factor do?

A

Links exposed collagen with platelets

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13
Q

What does fibrinogen do?

A

Forms platelet bridges –> occlusion

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14
Q

What does thrombin (Fx IIa) do?

A
  • Generates a more stable clot

- Converts fibrinogen –> fibrin

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15
Q

Which factors does thrombin (Fx IIa) activate?

A

F8

F5

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16
Q

What is the final result of the coagulation cascade?

A
  • Fibrinogen –> Fibrin

- Fibrin: seals hemostatic/ platelet plug

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17
Q

What are the 7 steps to platelet activation?

A
  1. Injury
  2. Collagen and vWF exposed
  3. Platelet adherence & activation
  4. Vasoconstrictors (i.e. TXA2) platelet recruiters (ADP), platelet activators (TXA2)
  5. Conformational change to IIb/IIIa receptor (on platelet surface)
  6. Binding of fibrinogen (crosslink platelets)
  7. Aggregation and platelet plug formation
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18
Q

What is the role of Serotonin in platelet activation?
Is serotonin a target of anti-platelet therapy?
What is the risk of SSRIs and clot formation?

A
  • Key role in platelet aggregation, vasoconstriction
  • NO
  • SSRIs carry an increased bleeding risk d/t its effects on platelet aggregation
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19
Q

What are the 3 key/ target factors in anti-platelet therapy?

A
  • ADP
  • TXA2
  • GPIIb/IIIa Receptor
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20
Q

What is the role of ADP?

A

Platelet activation

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21
Q

What is the role of an activated GPIIb/IIIa receptor?

A

When activated, binds fibrinogen

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22
Q

What are the 3 pathways of the coagulation cascade?

A
  • Intrinsic pathway
  • Extrinsic pathway
  • Common pathway
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23
Q

What is the intrinsic pathway activated by?

A

Damaged cells

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24
Q

What is the extrinsic pathway activated by?

A

Damaged vessel walls

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25
What is the common pathway? Which clotting factor does it start with?
- The convergence of the intrinsic/ extrinsic pathways | - Factor XA
26
What are the 3 key steps in the Extrinsic pathway of clotting?
1. Damaged endothelium/ tissue trauma produces TISSUE FACTOR 2. Tissue factor binds to FACTOR VII --> activates 3. Tissue Fx/ Fx VIIA complex activates Fx X --> FACTOR XA
27
What are the 5 key steps in the Intrinsic pathway of clotting?
1. Damaged cells produce POLY P 2. Poly P activates PRE-KALLIKREIN & FACTOR XII 3. Fx XIIA activates FACTOR XI 4. Fx XIA activates FACTORS IX & VIII 5. Factors VIIIA & IXA complex --> ACTIVATES Fx X --> FACTOR XA
28
What is the end product of both intrinsic/ extrinsic pathways of clotting?
Factor XA
29
What are the 3 key steps in the common pathway of clotting?
1. Factor XA converts Prothrombin (Fx II) to Thrombin (Fx IIA) 2. Thrombin converts FIBRINOGEN TO FIBRIN (ultimate goal) 3. Stable fibrin clot forms
30
What are some co-factors in the common pathway of clotting?
Ca2+ Platelet phospholipids Prothrombin activator
31
What is the role of anti-thrombin?
Can deactivate thrombin (Fx IIA) to prevent massive clotting
32
What does factor II do in the clotting cascade? Where does it act?
- Found in the common pathway aka Prothrombin | - Converted to thrombin (Fx IIA) by Factor XA
33
What does factor VII do in the clotting cascade? Where does it act?
- Binds to/activated by tissue factor to form a complex that will activate Fx XA - End of extrinsic pathway of clotting
34
What does factor IX do in the clotting cascade? Where does it act?
- Activated by Fx XIA to form a complex with Fx VIII | - Complex with Fx VIIIA activates Fx XA to end the intrinsic pathway of clotting
35
What does Factor X do in the clotting cascade? Where does it act?
- Factor X is activated in both the intrinsic & extrinsic pathways of clotting - Starts the common pathway of clotting by converting prothrombin (Fx II) to thrombin (Fx IIA)
36
What does Factor II do in the clotting cascade? Where does it act?
- Factor II aka Prothrombin is converted to Thrombin (Factor IIA) by Fx XA --> converts fibrinogen to fibrin - Start of the common pathway of clotting
37
What are the main 4 Factor targets of anticoagulant therapy?
Factors II, VII, IX and X
38
Which factors does Warfarin affect?
Factors II, VII, IX, and X (not yet-activated factors)
39
Which factors do heparin, enoxaparin (Lovenox), and fondaparinux affect?
Thrombin (IIA) and XA
40
Prothrombin time (PT) is the measurement of the activity of which factors? Variable?
- Measures activity of factors II, VII, IX, & X | - Yes, may vary from hospital to hospital
41
What is an INR? Which medication is this most reflective of?
- International Normalized Ratio is the same as PT but standardized worldwide - Key for warfarin
42
Partial thromboplastin time (PTT) is the measurement of the activity of which factors?
Factors II, V, VII, IX, X, XI, and XII
43
What are the 3 INDIRECT THROMBIN INHIBITORS?
- Unfractionated heparin (Heparin/ UFH) - Low molecular weight heparin (LMWH): enoxaparin (Lovenox) - Fondaparinux (Arixtra)
44
What is the MOA of an indirect thrombin inhibitor?
- Normal activity of antithrombin: binds factors IIA (thrombin), IXA, XA, XIA, and XIIA to inactivate them - Helps bridge anti-thrombin with thrombin to increase de-activation activity
45
Which 2 factors does unfractionated heparin de-activate?
Factors X and II (prothrombin)
46
What are 2 ways in which UFH can be administered? What are the indications?
- Continuous IV infusion for ACS and Warfarin bridging (acute VTE tx) - Subcutaneous injection: VTE prophylaxis
47
Which monitoring test should be used for UFH? Goal?
- aPTT | - Goal level is 2-2.5x control (baseline before heparin); approx 60-80 sec
48
What are 3 adverse effects of UFH?
- Bleeding - Heparin-Induced Thrombocytopenia (HIT) -- intolerance - Osteoporosis (long-term)
49
What is HIT? Potential complications?
- An antibody-mediated adverse effect of heparin (or enoxaparin) - It is strongly associated with venous & arterial thrombosis
50
How should you monitor a pt for HIT?
- If platelets fall >50% from baseline with nadir (lowest point) > 20K - If the platelets start to fall on days 5-10 of Rx - If thrombosis occurs while on heparin (abnormal!!) - Must R/O other causes of thrombocytopenia e.g. drugs: other antiplatelets, many antibiotics i.e. Zosin
51
What is the treatment for HIT?
STOP HEPARIN | Treat with an IV direct thrombin inhibitor
52
Describe the process behind HIT.
1. Heparin and Platelet Fx IV form a complex 2. Complex is seen as foreign, immune complex with IgG forms 3. Immune complex attaches to resting platelet on Fc receptor 4. Platelet activation --> thrombus formation --> decreased platelet count --> + feedback loop
53
What is the MC Low molecular weight Heparin?
Enoxaparin (Lovenox)
54
Which factors does enoxaparin inhibit?
Factors X and II (prothrombin), mostly Fx X
55
How is enoxaparin administered? Indications?
Subcutaneous injection for: - ACS - Warfarin bridging (acute VTE Rx) - VTE prophylaxis
56
How would you monitor enoxaparin?
- Not routinely monitored | - Could use Anti-XA level
57
What are 2 adverse effects of enoxaparin?
-Bleeding -NOT FOR PTS w/ severely reduced renal fxn: CrCl < 20mL/min REDUCE DOSE for pts w/ CrCl 20-30 mL/min
58
What are the commonalities between UFH and enoxaparin?
Both are used for ACE, acute VTE treatment and VTE prophylaxis
59
What are some benefits of using UFH over enoxaparin?
- UFH has a shorter half-life (1.5h vs. 7 hrs) -- used in surgery prep - Enoxaparin accumulates in renal dysfunction
60
What are some benefits of using enoxaparin over UFH?
- Enoxparain has a more predictable dose-response curve - Doesn't require routine monitoring - UFH therapeutic anticoagulation (ACS, VTE treatment) must be given as a continuous infusion; Lovenox would be preferred for outpatients (SQ)
61
Which factor does Fondaparinux inhibit?
Factor XA
62
How is Fondaparinux administered? Indications?
Subcutaneous injection for: - Acute VTE treatment - VTE prophylaxis - NOT FOR ACS
63
How is Fondaparinux monitored?
- Not routinely done! | - Anti XA level
64
What are 2 adverse effects of Fondaparinux?
- Bleeding | - NOT FOR PTS with renal dysfunction: CrCl <30 mL/min
65
How are INDIRECT thrombin inhibitors reversed?
1. D/C indirect thrombin inhibitor | 2. Protamine sulfate, given by IV infusion (binds to drug, deactivates it) --> Max dose 50 mg/10 min
66
What is the dose of protamine sulfate given for heparin?
1 mg/100 units heparin in the body
67
What is the dose of protamine sulfate given for enoxaparin? How effective is this?
1 mg/ mg enoxaparin in the body | -Only 60% effective
68
What is the dose of protamine sulfate given for fondaparinux?
NOT EFFECTIVE to reverse fondaparinux
69
What is the MOA of UFH? LMWH? Fondaparinux?
- UFH binds to antithrombin to help deactivate thrombin - LMWH binds to antithrombin partially affecting thrombin - Fondaparinux binds to antithrombin and stops thrombin from binding?
70
What are 2 Oral Direct Xa inhibitors?
- RivaroXABAN | - ApiXABAN
71
What are the indications for Rivaroxaban?
- VTE prophylaxis and treatment | - Prevention of stroke and systemic embolism in pts with nonvalvular ATRIAL FIBRILLATION
72
What are the indications for Apixaban?
- VTE prophylaxis after hip/knee replacement surgery | - Prevention of stroke and systemic embolism in pts with nonvalvular ATRIAL FIBRILLATION
73
What is the general MOA of Direct thrombin inhibitors (DTIs)?
-Binds directly to thrombin, action is INDEPENDENT of antithrombin
74
Name 2 IV DTIs and 1 PO DTI.
IV: Bivalirudin -Argatroban PO: Dabigatran
75
What are the indications for Bivalirudin?
- ACS undergoing PCI | - Anticoagulation in pts with HIT (after stopping heparin)
76
What are the indications for Argatroban?
- Anticoagulation in pts with HIT | - Coronary angioplasty in pts with HIT
77
How are the IV DTIs administered?
Continuous IV infusion
78
Which monitoring test should be used for the IV DTIs?
aPTT
79
What adverse effect is expected with the IV DTIs?
Bleeding
80
What reversal agent can be used against IV DTIs?
NONE: give supportive care (IV fluids) and blood products (e.g. packed RBCs)
81
What is the indication for Dabigatran (PO DTI)?
- -Prevention of stroke and systemic embolism in pts with nonvalvular ATRIAL FIBRILLATION - DVT prophylaxis and treatment
82
What is a major consideration for Dabigatran?
ACCUMULATES IN RENAL DYSFUNCTION -- may cause massive bleed - REDUCE dose if: CrCl 15-30 mL/min - DON'T USE if: CrCl <15 mL/min
83
Which monitoring test should be used for Dabigatran?
None
84
Which adverse effects are expected with Dabigatran?
- Bleeding | - G.I. upset
85
What reversal agent can be used against Dabigatran?
NONE; use dialysis
86
What is the MOA of Warfarin?
- Inhibits (inactive) factors II, VII, IX, X and proteins C and S (natural anticoagulants) - Vitamin K antagonist (precursor of activating clotting factors)
87
What are the indications of Warfarin?
- DVT/ PE treatment | - Prevention of stroke in pts with Afib or heart valve replacement
88
What is the monitoring test used for Warfarin? How many days would it take to become therapeutic on Warfarin? How is it usually initated?
- INR - Takes ~5 days to become therapeutic - Would need BRIDGE THERAPY d/t hypercoagulable state

Pharm II (5 decks)

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