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Questions and Answers
What is the main mechanism of action of GP IIb/IIIa antagonists?
What is the main mechanism of action of GP IIb/IIIa antagonists?
What is the typical recovery time for platelet function after discontinuation of a GP IIb/IIIa antagonist?
What is the typical recovery time for platelet function after discontinuation of a GP IIb/IIIa antagonist?
In which medical scenario are GP IIb/IIIa antagonists primarily used?
In which medical scenario are GP IIb/IIIa antagonists primarily used?
What is the term used for continuing a GP IIb/IIIa antagonist after discontinuation of another antiplatelet drug, such as Plavix, prior to surgery?
What is the term used for continuing a GP IIb/IIIa antagonist after discontinuation of another antiplatelet drug, such as Plavix, prior to surgery?
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Which of the following is NOT a commonly used GP IIb/IIIa antagonist?
Which of the following is NOT a commonly used GP IIb/IIIa antagonist?
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Which of the following is NOT a factor that Antithrombin III strongly inhibits?
Which of the following is NOT a factor that Antithrombin III strongly inhibits?
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Which of these anti-platelet agents acts by inhibiting cyclo-oxygenase?
Which of these anti-platelet agents acts by inhibiting cyclo-oxygenase?
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What is the mechanism of action of DDAVP in the treatment of von Willebrand's disease?
What is the mechanism of action of DDAVP in the treatment of von Willebrand's disease?
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Which of these drugs inhibits ADP-induced platelet aggregation?
Which of these drugs inhibits ADP-induced platelet aggregation?
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What is the purpose of administering protamine?
What is the purpose of administering protamine?
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What is the primary role of nitric oxide in a normal blood vessel?
What is the primary role of nitric oxide in a normal blood vessel?
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What happens to the blood vessel when it is injured?
What happens to the blood vessel when it is injured?
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What is the key factor involved in platelet adhesion to the exposed collagen in an injured blood vessel?
What is the key factor involved in platelet adhesion to the exposed collagen in an injured blood vessel?
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What is a characteristic feature of von Willebrand disease?
What is a characteristic feature of von Willebrand disease?
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What role does thrombin play in platelet activation?
What role does thrombin play in platelet activation?
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What are the key mediators released by activated platelets that promote further platelet aggregation?
What are the key mediators released by activated platelets that promote further platelet aggregation?
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How does thromboxane A2 contribute to platelet aggregation?
How does thromboxane A2 contribute to platelet aggregation?
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What is the key difference between the primary and secondary hemostasis?
What is the key difference between the primary and secondary hemostasis?
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What is the role of prostacyclin in hemostasis?
What is the role of prostacyclin in hemostasis?
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What is the key distinction between the platelet plug and a blood clot?
What is the key distinction between the platelet plug and a blood clot?
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What is the primary mechanism of action of thrombolytic agents?
What is the primary mechanism of action of thrombolytic agents?
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What is a common side effect or risk associated with thrombolytic therapy?
What is a common side effect or risk associated with thrombolytic therapy?
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Which of the following is a contraindication for the use of thrombolytic agents?
Which of the following is a contraindication for the use of thrombolytic agents?
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What is the primary indication for the use of thrombolytic agents?
What is the primary indication for the use of thrombolytic agents?
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What is a common cause of heparin resistance?
What is a common cause of heparin resistance?
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What is the most common organ where coumarin-like drugs exert their anticoagulant effect?
What is the most common organ where coumarin-like drugs exert their anticoagulant effect?
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How long should therapeutic doses of low molecular weight heparin (LMWH) be held before surgery?
How long should therapeutic doses of low molecular weight heparin (LMWH) be held before surgery?
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Which of the following is NOT a thrombolytic agent?
Which of the following is NOT a thrombolytic agent?
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What is the primary mechanism of action of heparin?
What is the primary mechanism of action of heparin?
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What is the primary source of unfractionated heparin?
What is the primary source of unfractionated heparin?
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Which anticoagulant is typically used for bridging therapy in patients on oral anticoagulants undergoing surgery?
Which anticoagulant is typically used for bridging therapy in patients on oral anticoagulants undergoing surgery?
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What factors can influence the effectiveness of heparin?
What factors can influence the effectiveness of heparin?
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Which of the following is a potential adverse effect associated with heparin use?
Which of the following is a potential adverse effect associated with heparin use?
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Which of the following is a common use of heparin in a perioperative setting?
Which of the following is a common use of heparin in a perioperative setting?
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Which of the following factors can contribute to heparin resistance?
Which of the following factors can contribute to heparin resistance?
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Why is it important to consider a patient's platelet count when administering heparin?
Why is it important to consider a patient's platelet count when administering heparin?
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Which of the following statements regarding heparin and pregnancy is CORRECT?
Which of the following statements regarding heparin and pregnancy is CORRECT?
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Why is preservative-free heparin recommended for pediatric use?
Why is preservative-free heparin recommended for pediatric use?
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What is the recommended interruption of therapeutic heparin before performing a neuraxial block?
What is the recommended interruption of therapeutic heparin before performing a neuraxial block?
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Why is regional anesthesia with low-dose heparin considered safe?
Why is regional anesthesia with low-dose heparin considered safe?
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What is the primary reason for monitoring for a neurological deficit after neuraxial anesthesia in patients receiving heparin?
What is the primary reason for monitoring for a neurological deficit after neuraxial anesthesia in patients receiving heparin?
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What is the primary role of antithrombin III in the action of heparin?
What is the primary role of antithrombin III in the action of heparin?
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Which of the following is NOT a common use of heparin in clinical practice?
Which of the following is NOT a common use of heparin in clinical practice?
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What is the active form of plasminogen?
What is the active form of plasminogen?
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What is the primary function of Protein S?
What is the primary function of Protein S?
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Which of the following is NOT a potential cause of acquired ATIII deficiency?
Which of the following is NOT a potential cause of acquired ATIII deficiency?
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What is the main mechanism of action of epsilon aminocaproic acid (EACA)?
What is the main mechanism of action of epsilon aminocaproic acid (EACA)?
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Which of the following is NOT a potential adverse effect of antifibrinolytics?
Which of the following is NOT a potential adverse effect of antifibrinolytics?
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What is the mechanism of action of protamine?
What is the mechanism of action of protamine?
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What is a potential risk associated with protamine administration?
What is a potential risk associated with protamine administration?
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What is the primary function of desmopressin (DDAVP)?
What is the primary function of desmopressin (DDAVP)?
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What is a potential adverse effect of desmopressin (DDAVP) administration?
What is a potential adverse effect of desmopressin (DDAVP) administration?
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Which of the following factors is NOT directly involved in the final common pathway of coagulation?
Which of the following factors is NOT directly involved in the final common pathway of coagulation?
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Which of the following is a potential cause of fibrinogen loss?
Which of the following is a potential cause of fibrinogen loss?
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What is the mechanism of action of recombinant activated factor VIIa (rFVIIa)?
What is the mechanism of action of recombinant activated factor VIIa (rFVIIa)?
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Which of the following recombinant proteins is used to stabilize the fibrin clot in the final common pathway of coagulation?
Which of the following recombinant proteins is used to stabilize the fibrin clot in the final common pathway of coagulation?
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What is a potential use for prothrombin complex concentrates?
What is a potential use for prothrombin complex concentrates?
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Which of the following is NOT a potential risk associated with high-dose tranexamic acid (TXA) administration?
Which of the following is NOT a potential risk associated with high-dose tranexamic acid (TXA) administration?
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Flashcards
PLT Recovery Time
PLT Recovery Time
The time required for platelet function to return to normal, typically 30 – 60 minutes.
GP IIb/IIIa Antagonists
GP IIb/IIIa Antagonists
Drugs like Abciximab, tirofiban, and eptifibatide that reduce thrombus formation.
Mechanism of GP IIb/IIIa Antagonists
Mechanism of GP IIb/IIIa Antagonists
They bind to fibrinogen receptors, blocking platelet aggregation.
Bridge Therapy
Bridge Therapy
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Platelet Function Recovery
Platelet Function Recovery
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Thrombolytic Agents
Thrombolytic Agents
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Plasminogen
Plasminogen
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Clot Lysis
Clot Lysis
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Indications for Thrombolytics
Indications for Thrombolytics
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Streptokinase
Streptokinase
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Hemorrhage
Hemorrhage
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Anesthetic Management
Anesthetic Management
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Neurological Assessments
Neurological Assessments
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Hemostasis
Hemostasis
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Vasodilation
Vasodilation
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Endothelial cells
Endothelial cells
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Platelet adhesion
Platelet adhesion
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Von Willebrand Factor
Von Willebrand Factor
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Thrombin
Thrombin
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Platelet activation
Platelet activation
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Thromboxane A2
Thromboxane A2
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Platelet aggregation
Platelet aggregation
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Temporary hemostasis
Temporary hemostasis
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Antithrombin III Function
Antithrombin III Function
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Heparin Action
Heparin Action
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ADP-Induced Platelet Aggregation Inhibitor
ADP-Induced Platelet Aggregation Inhibitor
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Desmopressin for von Willebrand’s Disease
Desmopressin for von Willebrand’s Disease
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Tranexamic Acid Function
Tranexamic Acid Function
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Antithrombin III
Antithrombin III
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Plasmin
Plasmin
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Tissue-type plasminogen activator (tPA)
Tissue-type plasminogen activator (tPA)
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Protein C
Protein C
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Protein S
Protein S
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Epsilon Aminocaproic Acid (EACA)
Epsilon Aminocaproic Acid (EACA)
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Tranexamic Acid (TXA)
Tranexamic Acid (TXA)
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Protamine
Protamine
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Desmopressin (DDAVP)
Desmopressin (DDAVP)
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Fibrinogen (Factor I)
Fibrinogen (Factor I)
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Recombinant activated factor VIIa (rFVIIa)
Recombinant activated factor VIIa (rFVIIa)
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Thrombus formation
Thrombus formation
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Antifibrinolytics
Antifibrinolytics
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Hypotension from protamine
Hypotension from protamine
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Fibrin split products
Fibrin split products
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Bleeding risk factors
Bleeding risk factors
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Unfractionated heparin
Unfractionated heparin
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Low molecular weight heparin
Low molecular weight heparin
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Heparin mechanism of action
Heparin mechanism of action
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Heparin resistance
Heparin resistance
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Heparin pharmacokinetics
Heparin pharmacokinetics
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Pregnancy & heparin
Pregnancy & heparin
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Heparin use in pediatrics
Heparin use in pediatrics
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Neuraxial anesthesia
Neuraxial anesthesia
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Therapeutic heparin
Therapeutic heparin
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Prophylactic heparin
Prophylactic heparin
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Fibrin and platelet activation
Fibrin and platelet activation
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Study Notes
Pharmacology of Anticoagulants & Procoagulants
- Anticoagulants and procoagulants are important drugs in managing bleeding and clotting disorders.
- Normal blood vessel endothelium releases nitric oxide causing vasodilation.
- Platelets adhere to exposed collagen to form a plug, a critical mechanism in primary hemostasis.
Physiology of Hemostasis
- Hemostasis is a complex process aimed at reducing or stopping bleeding.
- Primary hemostasis involves platelet activation, adhesion, and aggregation at the site of injury.
- Secondary hemostasis involves the activation of coagulation cascade culminating in cross-linked fibrin formation. This results in a stable clot.
- Clotting factors are proteins crucial for the coagulation cascade.
- Several different pathways contribute to the cascade (intrinsic pathway, extrinsic pathway, and final common pathway)
- These pathways are involved in clotting, but must be balanced with anti-coagulation mechanisms.
Overview of Hemostasis
- Normal healthy blood vessel walls maintain healthy blood flow and prevent blood clotting.
- Injured blood vessels expose collagen, triggering platelet adhesion and aggregation.
- In primary hemostasis, platelets form a plug.
- Platelets also release potent local vasoconstrictors.
- Secondary hemostasis involves clotting factors and the cascade leading to a fibrin clot.
Platelet Plug: Adhesion
- Subendothelial collagen exposure is a trigger for platelets to activate.
- Von Willebrand Factor (vWF) mediates platelet adhesion to subendothelial collagen.
- Von Willebrand disease affects vWF, leading to bleeding even with normal platelet counts.
Platelet Plug:Activation
- Platelet activation occurs when platelets come into contact with damaged endothelium.
- Thrombin also activates the platelets.
- Activated platelets release potent mediators such as thromboxane A2 and ADP.
- These mediators activate more platelets and promote aggregation.
Platelet Plug: Aggregation
- Thromboxane A2 from activated platelets uncovers fibrinogen receptors.
- Fibrinogen binds, linking platelets together, forming a temporary plug.
- Prostacyclin, a potent vasodilator and inhibitor of platelet activation, plays a counteracting role and prevents widespread clotting.
From PLT Plug to Stable Clot
- Platelets form a temporary aggregation, but this is followed by the coagulation cascade resulting in a stable fibrin clot.
- Coagulation factors work together to stabilize and strengthen this clot through complex and cascade-like reactions.
Secondary Hemostasis
- Secondary hemostasis involves the coagulation cascade, a complex series of reactions that lead to fibrin formation.
- The intrinsic pathway, extrinsic pathway, and the common pathway converge to allow fibrin formation.
Clotting Factors
- Various clotting factors are present in the coagulation cascade.
- Several factors are vitamin K-dependent.
- Some disorders are associated with deficiency of certain factors leading to bleeding.
3 Phase Cell-Based Coagulation Model
- Initiation, amplification, and propagation phases form a complex, coordinated response to initiate and then stabilize the clotting process.
- The extrinsic pathway is important in initiating the process and plays an essential role in clot formation.
- The intrinsic pathway is important to initiate the clot formation and stabilization process.
- The common pathway is important in formation and stabilization of the stable clot.
Coagulation Testing
- Common coagulation tests include PT (prothrombin time) and aPTT (activated partial thromboplastin time).
- These tests measure the time taken for blood to clot and evaluate the function of specific coagulation pathways.
- Interpretation of test results is often crucial in clinical practice when trying to determine blood disorders.
- PTT can be affected by several factors and has many different applications.
Activated Clotting Time (ACT)
- ACT is a test that measures the time it takes for blood to clot.
- Heparin and Protamine are important in managing this time.
Coagulation Tests
- Bleeding time, platelet count, thrombin time, and fibrinogen levels are other coagulation test parameters.
Thromboelastography (TEG), Thromboelastometry
- TEG/ROTEM are valuable techniques to assess the kinetics of clot formation and dissolution.
- These tests are often helpful in determining the optimal treatment path to take in cases of clotting disorders.
Pharmacology of Anticoagulants
- Anticoagulants are medications that prevent or slow blood clotting.
- Heparin is an anticoagulant; it can be unfractionated or low molecular weight.
- Unfractionated heparins are derived from porcine intestine or bovine lung.
- Low-molecular-weight heparins are produced in a way to remove the larger portions of the original unfractionated heparin, leading to a different chemical makeup.
- Heparin works by preventing thrombin from forming clots.
Heparin
- Unfractionated heparin and low-molecular-weight heparin (LMWH) are anticoagulants used to treat and prevent blood clots.
- Heparin increases the activity of antithrombin III, an important protein in neutralizing factors that drive clotting.
- LMWH are administered subcutaneously for more consistent blood clotting.
Heparin-Induced Thrombocytopenia (HIT)
- HIT is an adverse reaction to heparin that can cause thrombocytopenia (low platelet count) and thrombosis (blood clot formation).
Low-Molecular-Weight Heparin (LMWH)
- LMWHs are a class of anticoagulants that are more predictable and more specific in action than unfractionated heparin.
Warfarin
- Warfarin is an oral anticoagulant that inhibits the synthesis of vitamin K-dependent clotting factors.
Direct Thrombin Inhibitors
- Direct thrombin inhibitors directly block thrombin, preventing its conversion of fibrinogen to fibrin.
- Dabigatran is an example (Pradaxa)
Direct Factor Xa Inhibitors
- Rivaroxaban (Xarelto) and apixaban (Eliquis) are examples, directly inhibiting factor Xa.
Aspirin
- Aspirin irreversibly inhibits cyclooxygenase, preventing thromboxane A2 production and reducing platelet aggregation.
Clopidogrel (Plavix)
- Clopidogrel is a prodrug that irreversibly blocks the P2Y12 ADP receptor on platelets, inhibiting their activation and aggregation.
Antiplatelet Agents
- Antiplatelet agents are medications used to prevent blood clots by targeting platelet function.
- Aspirin and clopidogrel are commonly used antiplatelet agents.
Recombinant Proteins
- Recombinant proteins, like factor VIIa, can be used to manage critical bleeding episodes in specific situations.
- Factor XIII and prothrombin complex concentrates have roles in managing bleeding.
Topical Hemostatic Agents
- Topical hemostatic agents promote clot formation locally to control bleeding.
- These agents include topical thrombin, fibrin sealants involving fibrinogen and thrombin.
Thrombolytic Agents
- Thrombolytic agents dissolve existing blood clots.
Protamine
- Protamine is an antidote to heparin, neutralizing its anticoagulant effects.
Desmopressin (DDAVP)
- Desmopressin stimulates the release of von Willebrand Factor, addressing deficiencies in patients with bleeding issues.
Fibrinogen
- Fibrinogen is a clotting factor crucial for clot formation.
Recombinant Proteins
- Recombinant proteins, like factor VIIa and factor XIII, can be used to manage bleeding or clotting disorders.
Topical Hemostatic Agents
- Topical hemostatic agents promote faster clot formation at the site of the injury, reducing bleeding and promoting healing.
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Description
This quiz covers essential knowledge regarding GP IIb/IIIa antagonists, including their mechanisms of action, application scenarios, and recovery times for platelet function after discontinuation. Test your understanding of anti-platelet agents and their effects in clinical practice.