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51 Cards in this Set

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