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Pharmacology > Anticoagulation/AntiThrombotic Therapy > Flashcards

Anticoagulation/AntiThrombotic Therapy Flashcards

1
Q

Effects of thrombin

  1. Forms and ____ the ___ clot.
  2. Stimulates TAFI: what is this?
A

Effects of thrombin

  1. stabilizes; fibrin
  2. Thrombin Activated Fibrinolysis Inhibitor
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2
Q

Fibrolytic Pathway

  1. Activators converting plasminogen to plasmin?
  2. Inhibitors of plasminogen to plasmin conversion?
A

Fibrinolytic pathway

  1. Urokinase type plasminogen activator and tissue type
  2. Plasmin activator inhibitiors (PAI-I or PAI-II)
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3
Q

Fibrinolytic pathway

Inhibitors of plasmin itself?

A

Fibrinolytic pathway

a. Alpha1-antitrypsin
b. alpha2-antiplasmin
c. Thrombin-activatable fibrinolysis inhibitor

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4
Q

Anti-Platelet therapy:

Drugs?

A

Anti-Platelet therapy:

a. Aspirin
b. Thienopyridines
c. G IIb/IIIa receptor antagonists
d. PAR-1 inhibitor

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5
Q

Anti-Platelet therapy:

Aspirin:

  1. Mechanism of action?
  2. How can effects be reversed?
  3. Clinical implications?
A

Anti-Platelet therapy:

Aspirin:

  1. Irreversibly inhibits COX activity of PG synthesis
  2. Can only be reversed by new platelet generation
  3. Once daily dosing (and prolonged dissipation of anti-platelet effect)
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6
Q

Anti-Platelet therapy:

Thienopyridines:

Drugs?

A

Anti-Platelet therapy:

a. Ticlopidine
b. Clopidogrel
c. Prasugrel
d. Ticagrelor

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7
Q

Anti-Platelet therapy:

Thienopyridines (ticlopidine/clopidogrel/prasugrel/ticagrelor)

What do they inhibit? What is the result?

A

Anti-Platelet therapy:

Thienopyridines:

These are ADP receptor inhibitors and thus inhibit platelet aggregation

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8
Q

Anti-Platelet therapy:

Clopidogrel:

Mechanism of action?

How is it inactivated? What is this a problem with?

Peak level? Half life is longer than?

A

Anti-Platelet therapy:

Clopidogrel:

Irreversibly inhibits ADP binding to platelet P2Y12 receptor

Can only generate new platelets; issue with surgery

Peaks within an hour of ingestion; longer T1/2 than aspirin

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9
Q

Anti-Platelet therapy:

ADP receptor inhibitors:

  1. Intake of what is restricted when taking Ticagrelor?
  2. Who should not take Prasugrel?
A

Anti-Platelet therapy:

ADP receptor inhibitors:

  1. Aspirin intake, must be less than 100mg
  2. Patients over 76 or who weigh under 60kg shouldnt take prasugrel
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10
Q

Anti-Platelet therapy:

What drug had bad marketing on reduction in CVA patients?

A

Anti-Platelet therapy:

Vorapaxor

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11
Q

Anti-Platelet therapy:

Glycoprotein IIb/IIIa inhibitors:

  1. What does it bind to?
  2. What stage is it important for in platelet aggregation?
  3. What are the 3 in use? Route of administration?
A

Anti-Platelet therapy:

Glycoprotein IIb/IIIa inhibitors:

  1. vWF and fibrinogen
  2. Final common pathway
  3. Abciximab, Eptifibatide, Tirofiban; given IV only
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12
Q

Anti-Platelet therapy:

Abciximab:

  1. What is this? Function?
  2. Size? Duration of action?
  3. Binding?
A

Anti-Platelet therapy:

Abciximab:

  1. Fab fragment of ab against IIb/IIIa
  2. Large; Long duration of action
  3. nonspecific
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13
Q

Anti-Platelet therapy:

Eptifibatide and Tirofiban:

  1. Highly ___ and ___ inhibitors of what receptor?
  2. Half life? Speed of recovery of platelet function?
  3. ___% inhibition of platelet aggregation
A

Anti-Platelet therapy:

Eptifibatide and Tirofiban:

  1. Highly selective and reversible inhibitors of IIb/IIIa
  2. short half life; fast recovery of platelet function
  3. 80% inhibition of platelet aggregation
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14
Q

Anticoagulant classes:

  1. Inhibitors of clot initiation are blocking what pathway?
  2. Inhibitors of clot propagation are blocking what factor?
  3. Inhibitors of the fibrin formation are inhibiting?
A

Anticoagulant classes:

  1. VIIa/TF pathway (clot initiation)
  2. Factor Xa inhibitors (clot propagation)
  3. Direct thrombin inhibitors (fibrin formation)
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15
Q

Anti-Thrombosis:

Antithrombin agents (name 3)

A

Anti-Thrombosis:

Antithrombin agents:

a. Heparin
b. Low molecular weight heparin
c. Direct Thrombin inhibitors

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16
Q

Anti-Thrombosis:

Unfractionated Heparin:

  1. These are nonselective inhibitors of?
  2. Binds to?
  3. Elimination not dependent on?
A

Anti-Thrombosis:

Unfractionated heparin:

  1. Factor Xa inhibitors (inhibit clot propagation)
  2. Binds to endothelial cells and plasma proteins
  3. Elimination is not dependent on renal function
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17
Q

Anti-Thrombosis:

Unfractionated heparin:

  1. What does it stimulate? (that it doesnt want)
  2. What does it release? (that is good)
  3. What is its cofactor?
A

Anti-Thrombosis:

Unfractionated heparin:

  1. Simulates platelets and releases platelet factor 4
  2. Tissue factor pathway inhibitor
  3. Requires Anti-thrombin III as a cofactor
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18
Q

Anti-Thrombosis:

Antihemostatic effects of Heparin:

  1. What factors does it inactivate?
  2. Role in platelet function?
A

Anti-Thrombosis:

Antihemostatic effects of heparin:

  1. Inactivates factors IIa, IXa, Xa, and XIIa
  2. Inhibits platelet function and contributes to the hemorrhagic effects of heparin
19
Q

Anti-Thrombosis:

Limitations of Unfractionated Heparin:

  1. Unpredictable what?
  2. Narrow ____ window
  3. Reduced activity in the vicinity of ___ ____ ___
  4. It can also ___ clotting.
A

Anti-Thrombosis:

Limitations of UFH:

  1. Unpredictable anticoagulant response
  2. Narrow therapeutic window
  3. Reduced activity in the vicinity of platelet-rich thrombi
  4. It can also ACTIVATE clotting
20
Q

Anti-Thrombosis:

Advantages of LMWH vs. UFH:

  1. Administration?
  2. More ___ anticoagulant response.
  3. Half life?
  4. Lower incidence of _____.
A

Anti-Thrombosis:

Advantages of LMWH vs. UFH

  1. LMWH is easier to administer (subcutaneous not IV)
  2. More predictable anticoagulant response
  3. LMWH has a half life that is 2-4x longer
  4. Lowers the incidence of thrombocytopenia
21
Q

Anti-Thrombosis:

UFH:

This must be monitored: monitoring the therapeutic range with?

A

Anti-Thrombosis:

UFH:

PTT - Partial thromboplastin time

22
Q

Vitamin K Antagonists:

Name 6 drugs.

A

Vitamin K Antagonists:

a. Warfarin
b. Dicoumarol
c. Phenprocoumon
d. Indandione
e. Acenocoumarol
f. Anisindione

23
Q

Vitamin K Antagonists:

Warfarin:

  1. What factors and protiens are vitamin K dependent?
  2. These coagulation factors are biologically inactive unless ____ and this is dependend on ___ vitamin K
  3. What enzyme does warfarin inhibit?
A

Vitamin K Antagonists:

Warfarin:

  1. Factors II, VII, IX, and X as well as protein C and S are K depenent
  2. They are inactive unless decarboxylated which depends on reduction of vitamin K
  3. Vitamin K Oxide Reductase
24
Q

Vitamin K Antagonists:

Warfarin:

  1. Effect on already carboxylated molecules?
  2. Anticoagulant effect depends on depletion of ___ ___ in circulation.
A

Vitamin K Antagonists:

Warfarin:

  1. No effect on already carboxylated molecules
  2. Depends on depletion of carboxylated proteins in circulation (this depends on half lives)
25
Q

Vitamin K Antagonists:

Pharmacokinetics of Warfarin:

  1. Inter-individual sensitivity to warfarin is EXTREMELY ___.
  2. Intra-individual sensitivity is _____ affected by multiple factors: nutrition and ___ __ intake, gut ____, and ___.
A

Vitamin K Antagonists:

Pharmacokinetics of Warfarin:

  1. Interindividual sensitivity is EXTREMELY variable
  2. Intraindividual sensitivity is MARKEDLY affected by multiple factors: nutrition and vitamin K intake, gut flora, and medications
26
Q

Vitamin K Antagonists:

Problems with Warfarin:

  1. ______ dose response.
  2. ____ therapeutic range
  3. Bleeding?
  4. Monitoring?
  5. Reversibility?
A

Vitamin K Antagonists:

Problems with Warfarin:

  1. Unpredictable dose response
  2. Narrow therapeutic range
  3. High bleeding rate
  4. Difficult to monitor
  5. Slow reversibility
27
Q

Stroke in Atrial Fibrillation

In comparison to stroke without AF, how is stroke with AF?

A

Stroke in Atrial fibrillation

Strokes are more severe and disabling in patients with AF

28
Q

Risk factors for stroke in Non-valvular AF:

  1. Use _____ score.
  2. What is worth 1 point?
  3. What is worth 2 points?
A

Risk factors for stroke in Non-valvular AF:

  1. CHADS2 score
  2. CHF, hypertension, Age (75+), Diabetes
  3. Stroke or TIA in the past
29
Q

Antithrombic therapy in AF based on CHADS score:

What do you give for a patient with a score of:

  1. 0?
  2. 1?
  3. 2+?
A

Antithrombic therapy in AF based on CHADS score:

  1. Score of 0 = aspirin
  2. Score of 1 = Aspirin or Warfarin
  3. Score of 2+ = Warfarin
30
Q

Warfarin Dosing: monitored by?

A

Warfarin dosing is monitored by PT (prothrombin time) extrensic pathway

31
Q

Pentasaccharide:

Mechanism of action:

Produces an irriversible ____ change in ____, which binds to and inhibits factor ____. It thus inhibits clot ______.

A

Pentasaccharide:

Produces an irreversible conformational change in antithrombin which binds to and inhibits factor Xa. It thus inhibits clot propagation

32
Q

Fondaparinux:

  1. Indirect inhibition of Factor ___. This is via ____.
  2. ____ selective.
  3. ____ inhibit thrombin activity
  4. ____ inhibit thrombin generation
  5. FDA approved for?
A

Fondaparinux:

  1. Indirect inhibition of Factor Xa. This is via AT-III
  2. Highly selective
  3. DOESNT inhibit thrombin activity
  4. DOES inhibit thrombin generation
  5. FDA approved for DVT prophylaxis in hip fracture, TKA/THA (Total hip/knee arthroplasty)
33
Q

Direct Thrombin Inhibitors:

What ones are bivalent?

What ones are Univalent?

A

Direct Thrombin Inhibitors:

Bivalent - Hirudin and Bivalirudin

Univalent - Argatroban, dabigatran, ximelagatran

34
Q

Potential advantages of direct inhibitors:

  1. Affect only one factor: ___
  2. Independent of ____
  3. Inhibition of thrombin-mediated activation of?
  4. Active against what types of thrombin?
A

Potential advantages of direct inhibitors

  1. Thrombin
  2. Independent of AT-III
  3. Inhibition of activation of clotting factors (V, VIII, and XIII) and platelets
  4. *****Active agains free and clot-bound thrombin
35
Q

Which direct thrombin inhibitors are given IV?

Which are given orally?

A

Bivalirudin and Argatroban are IV

Ximelagatran and Dabigatran are oral

36
Q

Bilavirudin:

  1. Partially ____ binding
  2. No inhibition of thrombin ____
  3. FDA approved for?
  4. Direct ____ thrombin binding.
A

Bilaviruden:

  1. reversible
  2. NO inhibition of thrombin generation
  3. FDA approved for anticoagulation during PCI (Percutaneous coronary intervention)
  4. Direct bivalent binding
37
Q

Argatroban

  1. Type of binding?
  2. Excretion?
  3. FDA approval for treatment of?
A

Argatroban

  1. Reversible competitive binding
  2. Hepatic excretion
  3. FDA approval to treat HIT and for PCI in patients with a history of HIT (Heparin Induced Thrombocytopenia)
38
Q

New oral Anticoagulants:

What two new drugs are Direct Xa inhibitors used for DVT and nonvalvular Afib?

What is Pradaxa? For?

A

New oral anticoagulants:

Xarelto and Eliquis (Direct Xa inhibitors)

Pradaxa - direct thrombin inhibitor for nonvalvular Afib and DVT

39
Q

Fibrinolytic Therapy:

  1. TPA is released from endothelial cells but rapidly cleared by?
  2. What is protected from inhibition?
A

Fibrinolytic Therapy:

  1. Cleared by PAI-1 and PAI-II
  2. Fibrin-bound plasmin is protected from inhibition
40
Q

Fibrinolytic Therapy:

Agents? (4)

A

Fibrinolytic Therapy:

a. Streptokinase
b. Reteplase
c. Tenecteplase (TNK)
d. Wild-type TPA

41
Q

Fibrinolytic Therapy:

Wild-type t-PA:

  1. Activates what kind of plasminogen?
  2. Route of administration?
  3. Half life?
A

Fibrinolytic Therapy:

Wild-type t-PA:

  1. Activates bound plasminogen several hundred-fold more rapidly than circulating plasminogen
  2. IV (continuous infusion)
  3. Very short
42
Q

Fibrinolytic Therapy:

All fibrinolytic agents have the ptoential to cause?

A

Fibrinolytic Therapy:

All can cause very serious bleeding including a very small incidence of intracranial hemorrhage

43
Q

Clinical role for lytics?

A

Acute MI, stroke, pulmonary emboli, declot IV catheters/dialysis accesses, and DVT

Pharmacology (24 decks)

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