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51 Cards in this Set
- Front
- Back
GP1b alpha
(Glycoprotein 1b alpha) |
Platelet receptor for vWF.
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TXA2
(thromboxane A2) |
Released by activated platelets to activate others.
Binds the platelet TXA2 receptor. |
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P2Y1 & P2Y12
(purinergic receptors) |
Platelet receptors for ADP.
Ligand binding activates platelet at site of injury. |
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ADP
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Released by activated platelets to activate others.
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Par1 & Par4
(protease activated receptors) |
Platelet receptors for thrombin.
Ligand binding induces activation. |
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alpha2A adrenergic receptor
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Platelet receptor for epinephrine.
Ligand binding induces activation. |
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PGI2
(prostaglandin I2) |
Binds platelet receptor to inhibit activation.
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GPIIb-IIIa
(glycoprotein IIb- IIIa) |
Platelet receptor for fibrinogen.
Tethers 2nd layer of platelets. |
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Glanzmann thrombasthenia
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Defect in platelet fibrinogen receptor GPIIb-IIIa.
Bleeding disorder. |
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vonWillebrand disease
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Defective in vWF.
Bleeding disorder. |
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Bernard-Soulier syndrome
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Defect in platelet receptor for vWF, GP1b alpha. Deffective platelet aggregation, giant platelets.
Bleeding disorder. |
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Fibrinogen
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Cleaved by thrombin into fibrin and fibrinopeptides (from amino-terminal of alpha and beta chains).
6 peptide chains (2 alpha, 2 beta, 2 gamma). Very prevalent in blood normally. |
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Factor XIIIa
alpha2-AP |
Stabilizes fibrin network by forming covalent bonds (cross-linking).
Released from platelets in clot. Activity is regulated by thrombin. |
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Factor VII
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Extrinsic pathway.
Circulates in blood. Contacts TF. Activates factor X. |
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TF
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Tissue factor, produced by non-endothelial cells in vascular wall when injury occurs.
Activates factors VII & X. Membrane-bound protein. |
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AT
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Antithrombin.
Serine protease inhibitor of thrombin and factor Xa. Forms TAT complex with thrombin, with is 1000x more likely in presence of heparin. |
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TFPI
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Tissue factor pathway inhibitor.
Inhibits the initiation complex of coagulation between TF and factors VIIa and Xa. |
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Protein C
APC |
Anticoagulant pathway, activated protein C.
Circulates, is cleaved by thrombin bound to thrombomodulin. With protein S, inactivates tenase and prothrombinase by cleaving VIIIa and Va. |
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APC resistance
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Defect in coagulation factor V (fV Leiden mutation).
Thrombotic disorder, most common in caucasians. Factor V is resistant to inactivation by APC. |
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Plasmin
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Fibrinolysis.
Cleaves insoluble fibrin into soluble fibrin degradation products, fragments D-dimer and E, which are measured in patient's plasma. Destroys factors V, VIII, and XII. |
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uPA & tPA
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Urokinase-type plasminogen activator & tissue-type.
Converts plasminogen to plasmin. Given in drug form. tPA is released by damaged tissues once plasminogen gets trapped in clot. |
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PAI-1
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Plasminogen activator inhibitor 1.
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Staphylokinase & streptokinase
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Bacterial activators of plasminogen.
Given in drug form. |
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Recombinant factor VIII
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Most common drug therapy for bleeding disorders.
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Thrombocytopenia
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Bleeding disorder, mostly in small vessels, since platelets are the primary clotting factors there.
Platelet count below 50,000, and below 10,000 is lethal. Treatment: whole blood or spleenectomy to cease platelet removal. |
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Purified factor VII
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Given to trauma patients to limit blood loss & brain hemorrhage.
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Prothrombin
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Plasma protein, alpha2-globin.
Vit. K dependent synthesis. Converted to thrombin by factor Xa. |
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Factor Va
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Not proteolytic, but binds factor Xa and enhance's Xa's activity of thrombin formation.
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Prothrombinase
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Factor Xa + factor Va + platelets + calcium.
Amplified by thrombin. Formation of prothrombinase is the rate-limiting step of clotting. |
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Tenase
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Factor VIIIa + factor IXa + platelets + calcium.
Amplified by thrombin. |
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Vitamin K dependant factors
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Coagulation: prothrombin, factors VII, IX, and X.
Anticoagulation: protein C and protein S. Vitamin K is made by intestinal bacteria and used in liver. |
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HMW Kininogen
(high molecular weight) |
Intrinsic pathway activator.
Produces factors XIIa and XIa. |
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Thrombin
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Cleaves fibrinogen to fibrin and prothrombin to more thrombin.
Also activates factors VIII, IX, X, XI, and XII. Activated from prothrombin by prothrombinase complex. |
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Kallikrein
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Activates factor XII in intrinsic pathway.
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endogenous platelet activation inhibitors
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PGI2, Ecto-ADPase, NO.
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Thrombophilia
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Excessive clotting.
Factor V Leiden mutation or deficiency of protein C or S. |
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Hemophilia A & B
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A: Factor VIII deficiency
B: Factor IX deficiency (Christmas disease). X-linked recessive, common in men. |
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Stasis
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Hypercoagulable state.
Huge clots form in legs when legs are propped up for long time periods. PE when pieces break off. Treatment: tPA |
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Disseminated intravascular coagulation
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Widespread clotting due to large amounts of dying tissue (releases TF) or sepsis.
Vessel blockage can lead to circulatory (septic) shock. |
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Coumadin/Warfarin
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Anticoagulant.
Inhibits gamma-carboxylation of Vitamin K dependent factors. This decreases production by liver of clotting factors and prothrombin. |
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Heparin
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Anticoagulant.
Enhances antithrombin activity. |
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Hirudin/hirulog
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Anticoagulant.
Inhibits thrombin. |
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GPIIb-IIIa blocking antibodies
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Antiplatelet.
Blocks fibrinogen receptors. |
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COX inhibitors (NSAIDS, steroids) or phospholipase inhibitors
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Antiplatelet.
Inhibit TXA2 biosynthesis. |
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Ticlopidine, Clopidogrel
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Antiplatelet.
Blocks ADP receptor. |
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Factor X
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Common pathway.
As prothrombinase, activates prothrombin to thrombin. Activated by factor VIIIa. |
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Factor XII
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Intrinsic pathway.
Activated by kallikrein and HMW kininogen. Converts factor XI to XIa. |
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Factor XI
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Intrinsic pathway.
Activated by factor XIIa and HMW kininogen. Converts factor IX to IXa. |
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Factor IX
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Intrinsic pathway.
Activated by factor XIa. Part of Tenase, converts factor X to Xa. |
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Factor VIIIa
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Intrinsic pathway.
Part of tenase, converts factor X to Xa. |
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Factor Va
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Common pathway.
Part of prothrombinase, converts prothrombin to thrombin. |