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Pharmacology fall 2024 > Coagulation (Exam IV) > Flashcards

Coagulation (Exam IV) Flashcards

1
Q

What two factors are exposed by injury leading to platelet adherence & activation?

A

-Exposed Collagen
- Von Willebrand Factor

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2
Q

What type of thrombus is associated with a high pressure vessel (i.e. artery)?

A

White Thrombus (No RBCs, just fibrin)

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3
Q

What type of thrombus is associated with a low pressure vessel (i.e. vein)?

A

Red Thrombus (RBC + fibrin)

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4
Q

What do platelets release that. causes local vasoconstriction?

A

Serotonin

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5
Q

What type of thrombus would you expect to see associated with Coronary Artery Disease? Why?

A

White Thrombus (high pressure vessel, no RBCs)

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6
Q

Detachment of Red thrombi typically leads to what complication?

A
  • Pulmonary Embolism
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7
Q

DVT risk factors can be _________ and/or _________.

A
  • Inherited; acquired
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8
Q

What are some examples of inherited DVT risk factors?

A
  • Antithrombin III deficiency
  • Protein C or S deficiency
  • Sickle Cell Anemia
  • Activated Protein C resistance
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9
Q

What are some examples of acquired DVT risk factors?

A
  • Bedbound
  • Surgery/trauma
  • Obesity
  • Estrogen use (birth control typical)
  • Malignancies
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10
Q

What common form of transportation is a risk factor for DVT formation? How is this prevented?

A
  • Airplane flights
  • Getting up, stretching, flexing lower extremities.
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11
Q

What is DIC? Why does this occur?
What results from this condition?

A
  • Disseminated Intravascular Coagulation
  • Completely used up blood clotting factors
  • Excessive spontaneous bleeding is the result.
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12
Q

What are four common causes of DIC?
What are the treatments?

A
  1. Massive tissue injury
  2. Malignancy
  3. Bacterial Sepsis
  4. Abruptio Placentae

Plasma transfusion & treatment of underlying cause.

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13
Q

What is the mortality of DIC?

A
  • 10-50%
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14
Q

How is overcoagulation avoided by our body’s internal mechanisms?

A

Regulation of Coagulation via:
- Fibrin Inhibition
- Fibrinolysis

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15
Q

What 4 protease inhibitors rapidly inactivate coagulation proteins?

A
  1. α1 antiprotease
  2. α2 macroglobulin
  3. α2 antiplasmin
  4. Antithrombin
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16
Q

What enzyme converts plasminogen to plasmin?
What is the purpose of this conversion?

A
  • tPA (tissue Plasminogen Activator)
  • Plasmin actually breaks down the clot itself
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17
Q

What drug protects a clot from lysis via plasmin?

A
  • Aminocaproic acid
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18
Q

Which three enzymes potentiate the fibrinolytic process?
How do they accomplish this?

A
  1. t-PA
  2. Urokinase (produced in kidneys)
  3. Streptokinase

Conversion of plasminogen to plasmin.

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19
Q

What are the four groups of coagulation modifying drugs?

A
  1. Anticoagulants
  2. Antiplatelets
  3. Thrombolytic (Fibrinolytics)
  4. Hemostatic/Antifibrinolytics
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20
Q

Differentiate anticoagulants & antiplatelets.

A
  • Anticoagulants - Inhibit action or formation of clotting factors thus preventing clot formation.
  • Antiplatelets - Inhibit platelet aggregation thus preventing platelet plugs.
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21
Q

What is the prototypical parenteral anticoagulant drug & its general MOA?
What is the goal of therapy with this drug?

A
  • Heparin = inactivation of clotting factors
  • Goal = ↓ venous thrombosis
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22
Q

What is the prototypical oral anticoagulant drug & its general MOA?
What is the goal of therapy with this drug?

A
  • Warfarin = ↓ synthesis of clotting factors
  • Goal = ↓ venous thrombosis
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23
Q

What is the prototypical oral antiplatelet drug & its generalized MOA?
What is the goal of therapy with this drug?

A
  • Aspirin - ↓ platelet aggregation
  • Goal = ↓ arterial thrombosis
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24
Q

What is the prototypical thrombolytic drug?

A

Streptokinase

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25
Q

What drugs are indirect thrombin inhibitors?
What is their MOA?

A
  • Unfractionated & fractionated forms of heparin
  • Enhances anti-thrombin activity, inactivation of factor Xa, & inhibition of thrombin.
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26
Q

Differentiate unfractionated heparin, LMW heparin, & Fondaparinux.

A
  • Unfractionated Heparin = ↑ Antithrombin III activity, binds to ATIII, Xa, & Thrombin.
  • LMW Heparin = Binds to Xa, & ATIII
  • Fondaparinux = binds to ATIII only (via pentasaccharide sequence)
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27
Q

What enzyme does heparin activate?
How much does heparin enhance this enzyme’s activity?
At what rate is the heparin consumed through this process?

A
  • Antithrombin III (via conformational change)
  • 1000x enhancement
  • Heparin is not consumed by this process, only acts as a catalyst.
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28
Q

What molecular weight (MW) would you expect of unfractionated heparin?

A
  • 5000 to 30,000
29
Q

Where is unfractionated heparin derived from?

A
  • Pig (porcine) intestine and/or cow (bovine) lung
30
Q

Which heparin is more specific for factor Xa?
What does this mean for its efficacy?

A
  • LMW heparin (enoxaparin)
  • Less anticoagulative efficacy due to no binding on thrombin itself.
31
Q

When would a LMW heparin be chosen over an unfractionated heparin?

A
  • If an allergy to unfractionated heparin is present.
32
Q

What are the two possible complications associated with heparin toxicity?

A
  • Bleeding
  • Transient thrombocytopenia (HIT)
33
Q

With what heparin is the risk of HIT (heparin-induced thrombocytopenia) higher?
What is the basic pathophysiology of HIT?

A
  • Unfractionated.
  • Transient ↓PLTs (platelets) due to antibodies binding to heparin-PLT complex and immune system destruction of PLTs.
34
Q

Who is more prone to hemmorrhage associated with heparin toxicity?

A
  • Elderly women & renal failure patients
35
Q

What lab value is utilized to monitor proper anticoagulation levels when utilizing heparin?

A

aPTT (activated Partial Thromboplastin Time)

36
Q

Which lab test evaluates the extrinsic system of the coagulation cascade?

A
  • Prothrombin time (PT/INR)
37
Q

Describe a PT/INR test.

What is a normal INR?

A
  • Tissue Factor III is added to the blood. The time to clot (PT) is measured & compared to a control (INR).
  • Normal INR is 1
38
Q

What does aPTT measure?
What is added to this test to get this measurement?
What is a normal aPTT?

A
  • Activity of intrinsic system & common pathway
  • Phospholipids are added.
  • 35 - 45s
39
Q

What drug is given to reverse heparin?
What is this drugs MOA?
What is this drug’s effects on enoxaparin & fondaparinux?

A
  • Protamine Sulfate
  • very + charge and binds to - charge heparin
  • Small effect on LMW heparin & no effect on fondaparinux
40
Q

What is Fondaparinux?
What is it selective for?
When is this drug useful?

A
  • Pentasaccharide molecule of heparin.
  • Selective for Antithrombin & factor X.
  • Useful for HIT
41
Q

Which direct thrombin inhibitors bind to both active & substrate sites of thrombin?
Which direct thrombin inhibitors bind only to thrombin active sites?
What animal do we derive these drugs from?

A
  • Hirudin & Bivalirudin
  • Argatroban, Melagatran, & Dabigatran
  • Direct thrombin inhibitors derived from leeches.
42
Q

What is the bioavailability of warfarin?
Protein binding?
T½?

A
  • 100% bioavailable
  • 99% protein bound?
  • T½ = 36 hours
43
Q

What is warfarin’s mechanism of action?

A

Blocks Vitamin K reductase from converting prefactors into factors.

needs verification & better explanation

44
Q

What is the delay in onset of action of warfarin?
What does this mean clinically?

A
  • 8-12 hours till effect is seen
  • Wean off of heparin & on to warfarin slowly.
45
Q

What toxicity is seen with warfarin overdosing?

A
  • Bleeding
  • Hemmorhagic disorder of fetus & birth defects
  • Cutaneous necrosis
46
Q

What is a normal INR?
What is the target INR with warfarin therapy?

A
  • 0.8 - 1.2
  • Target: 2-3
47
Q

The goal of warfarin therapy is reduction of prothrombin activity by ______ %.

A

25%

48
Q

What is the consequence of warfarin’s rate of protein binding?

A
  • Warfarin protein binding rate (99%) can antagonize binding of other drugs.
    ex. Phenytoin can be displaced by warfarin thus causing phenytoin toxicity.
49
Q

What would be given to reverse warfarin?

A
  • Stopping warfarin
  • Large dose of Vitamin K
  • FFP or Factor concentrates
50
Q

What reversal is available for all the -aban drugs? (apixaban, rivaroxaban, etc.)
How do these drugs work?

A
  • No reversal is available.
  • Inhibition of Factor Xa & Thrombin
51
Q

How do virtually all fibrinolytic drugs work?

A
  • Catalyze the formation of Plasminogen into plasmin.
52
Q

Differentiate streptokinase & urokinase.

A
  • Urokinase is synthesized by the kidneys & streptokinase is synthesized by streptococci. Both break down clots directly via catalyzation of plasminogen into plasmin
53
Q

How does t-PA differ from other fibrinolytics?

A
  • t-PA preferentially activates plasminogen that is bound to fibrin avoiding systemic fibrinolysis and focusing on formed thrombus.
54
Q

What is aspirin’s mechanism of action?

A

Inhbition of TXA₂ via inhibition of COX pathway.

55
Q

What is the mechanism of action of clopidogrel & Ticlopidine?
Which of these two is associated with thrombocytopenic purpura?

A
  • Irreversible inhibition of ADP receptor on platelets. This prevents eventual platelet interbinding using GP IIb/IIIa receptors.
  • TTP associated with Ticlopidine.
56
Q

How does Plavix (clopidogrel) compare in efficacy to aspirin?

A
  • Well. 8.7% reduction in ischemic events vs aspirin only.
57
Q

Where do Monoclonal antibody anti-platelet
drugs work?
Name the prototypical drug of this class.

A
  • Targeting of IIb/IIIa receptors on platelet, thus preventin platelets from adhering to each other using fibrin.
  • Abciximab
58
Q

What phosphodiesterase inhibitor prevents platelet aggregation?

A

Cilostazol

59
Q

What antiplatelet drug inhibits adenosine uptake & cGMP phosphodiesterase activity & is used as an adjunct with other therapies?

A

Dipyridamole

60
Q

Where does Vitamin K confer its effects to upregulate blood coagulation?

A
  • Prothrombin
  • Factors VII, IX, & X
61
Q

What does Desmopressin Acetate treat?
How does it work?

A
  • Hemophilia A & von Willebrand Disease
  • ↑ Factor VIII activity
62
Q

Which drugs inhibit fibrinolytic activity? How?

A
  • Aminocaproic & Tranexamic Acid inhibit fibrinolysis by preventing the conversion of plasminogen to plasmin.
63
Q

What is Tranexamic acid used for?

A
  • Decreasing bleeding in Trauma, heavy menstruation, & epistaxis.
64
Q

What links platelets together to form the platelet plug?
What receptors are used to accomplish this?

A
  • Fibrinogen
  • GP IIb/IIIa receptors on the platelet.
65
Q

What drug class is Abciximab?

A

Monoclonal Antibody GP IIb/IIIa Inhibitor

66
Q

What is Virchow’s Triad?

A
  • Endothelial Injury
  • Stasis
  • Hypercoagulability
67
Q

What two things are exposed by an endothelial cell injury?

A

Collagen & vWF

68
Q

What do Collagen and vonWillebrand factor interact with once exposed by injury?

A
  • GP 1a & 1b receptors on the Platelet.
69
Q

What occurs with platelet GP 1a & 1b receptor activation?

A
  • ADP, Thromboxane, & Serotonin are released & cause platelets to use GP IIb/IIIa receptors & fibrin to stick together.

Pharmacology fall 2024 (23 decks)

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