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3 initial responses to vascular injury
vasoconstriction, platelet adhesion, thrombin generation
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exposed collagen + prekallikrein + HMW kininogen + factor XII
intrinsic coagulation pathway
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tissue factor (injured cells) + factor VII
extrinsic coagulation pathway
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factor X + factor V + Ca + platelet factor 3 + prothrombin
prothrombin complex
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catalyzes formation of thrombin
prothrombin complex
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convergence point for intrinsic and extrinsic pathways
Factor X
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inhibitor of factor X
tissue factor pathway inhibitor
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combines with platelets to form platelet plug to cause hemostasis
fibrin
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factor that helps crosslink fibrin
XIII
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factor that converts fibrinogen to fibrin + fibrin split products
thrombin
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factor that activates platelets
thrombin
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factor that activates factors V and VIII
thrombin
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factor with the shortest half-life
factor VII
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labile factors that are lost in stored blood. activity is not lost in FFP
Factors V and VIII
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only clotting factor not synthesized in liver
Factor VIII
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Vitamin K dependent factors (4 + 2)
II, VII, IX, and X. Also proteins C and S.
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length of time it takes Vitamin K to take effect
6 hours
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length of time FFP is effective after administration
6 hours
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other name for factor II
prothrombin
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normal half life of RBCs
120 days
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normal half life of platelets
7 days
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normal half life of PMNs
1-2 days
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anticoagulation factor that binds and inhibits thrombin
antithrombin III
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anticoagulation factor that degrades factors V and VIII, and fibrinogen
Protein C
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anticoagulation factor that acts as a cofactor to Protein C
Protein S
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factor that heparin binds to inhibit coagulation
antithrombin III
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fibrinolytic that is released from the endothelium and converts plasminogen to plasmin
tissue plasminogen activator (TPA)
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fibrinolytic factor that degrades factors V and VIII, fibrinogen and fibrin to degrade platelet plugs
plasmin
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fibrinolytic natural inhibitor of plasmin, released from the endothelium
alpha-2 antiplasmin
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factor secreted by platelets to increase platelet aggregation and promote vasoconstriction
thromboxane A2 (TXA2)
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enzyme secreted by endothelium that decreases platelet aggregation and promotes vasodilation
prostacyclin I2 (PGI2)
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blood product containing highest concentration of vWF, VIII, fibrinogen
cryoprecipitate
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blood product with high levels of factor V, VIII, protein C, protein S, ATIII
FFP (contains all factors)
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drugs (2) that cause release of factor VIII and vWF from endothelium
DDAVP, conjugated estrogens
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coagulation measurement of factors II, V, VII, X
PT
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best lab value to measure synthetic liver function
PT
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lab value measuring most factors (except VII and XIII)
PTT
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ACT level desirable for routine anticoagulation
150-200
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ACT level desired for cardiopulmonary bypass
350-400
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most common congenital bleeding disorder
Von Willebrands disease
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congenital bleeding disorder with normal PT, typically normal PTT, and long bleeding time
Von Willebrands disease
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bleeding disorder with a defective Gp1b receptor on platelets, causing them to have decreased linkage to collagen
Von Willebrands disease
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treatment for Von Willebrands (3)
cryoprecipitate, DDAVP, conjugated estrogens
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reduced circulating vWF
Type I vWD
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defect in vWF molecule itself
Type II vWD
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congenital deficiency in factor VIII. prolonged PTT, normal PT
Hemophilia A
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treatment of hemophilia A bleeding
factor VIII concentrate, cryoprecipitate
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congenital deficiency in factor IX
Hemophilia B (Christmas disease)
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treatment of hemophila B bleeding
factor IX concentrate, cryoprecipitate
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generic cause of bruising, epistaxis, mucosal bleeding, petechiae, purpura
platelet disorders
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GpIIb/IIIa receptor deficiency on platelets which blocks them from binding each other
Glanzmann's thrombocytopenia
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Gp1b receptor deficiency of platelets that keeps them from binding collagen
Bernard Soulier disease
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inhibits Gp1b, GpIIb/IIIa, vWF
Uremia
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treatment of uremic platelet dysfunction (4)
hemodialysis, DDAVP, cryoprecipitate, platelets
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drug that acts as an ADP receptor antagonist, causes platelet dysfunction
Plavix
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antibiotics that bind platelets and increase bleeding time (2)
PCN, cephalosporins
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thrombocytopenia due to antiplatelet antibodies
HIT (heparin induced thrombocytopenia)
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coagulation disorder characterized by decreased platelets, prolonged PT and PTT, and low fibrinogen. often initiated by tissue factor
DIC
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drug that inhibits cyclooxygenase in platelets, decreasing TXA2
aspirin
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most common congenital hypercoagulability disorder, causing 30% of spontaneous venous thromboses
Leiden factor
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defect in platelet function causing thrombosis and also bleeding. treatment: ASA
Polycythemia vera
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disorder with prolonged PTT, positive Russel viper venom time, false positive RPR for syphilis
Lupus anticoagulant
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causes of acquired hypercoagulability (6)
tobacco, malignancy, inflammatory bowel disease, OCPs, pregnancy, post-surgery
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decrease of protein C and S compared to procoagulation factors, leading to a relatively hyperthrombotic state
warfarin induced skin necrosis
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treatment of 1st DVT
warfarin 6 months
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treatment of 2nd DVT
warfarin 1 year
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treatment of 3rd+ DVT or any PE
lifetime warfarin
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drug that prevents decarboxylation of glutamic residues on Vitamin K dependent factors.
Warfarin
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drug that inhibits platelets and coagulation factors
dextran
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treatment to improve venous return and induce fibrinolysis via tPA release
SCDs
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drug that activates antithrombin III
heparin
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drug used to reverse heparin action
protamine sulfate
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drug that inhibits fibrinolysis by inhibiting plasmin; used in DIC or post-cardiopulm bypass
aminocaproic acid (Amicar)
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absolute contraindications to thrombolytic use (3)
active bleeding, recent (<2months) CVA, intracranial pathology
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