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 Introduction
 Coagulation mechanism
 Coagulation factors
 Intrinsic pathway
 Extrinsic pathway
 Fibrinolytic system
 Laboratory test for secondary hemostasis

Secondary hemostasis - coagulation cascades and lab tests

FIBRINOGEN
 Level is greatest among coagulation proteins.
 Three pairs of polypeptides – Aa,Bb and gamma – held
by disulphide bonds.
 Three domains : two outer D domains and one central
E domain.
 Fibrinopeptides A and B are located in central E
domain.
 Also an acute phase reactant protein.

PROTHROMBIN
Converted to thromin by prothrombinase.

THROMBOPLASTIN
 Required for activation of FvII.
 Composed of protein and phospholipid.
 Max concentration in brain,placenta and lungs.

LABILE FACTOR
 Heat labile. Inactivated at room temperature rapidly.
 Activated by thrombin
 Stored in platelet alpha granules – released from
activated platelets.
 Prothrombinase complex

STABLE FACTOR
 Tissue injury – complex between single chain form of
factor vII, tissue factor and calcium – generates Xa
from X.
 Factr Xa then in reverse reaction cleaves FVII to FVIIa.
 Also activates FIX

ANTIHEMOPHILIC FACTOR
 Circulates in plasma as noncoavalently bound complex
of two components : FVIIIc and vWf.
 FVIII : LMW, has procoagulant activity and is Xlinked.
 Gene for it is on long arm X chromosome.
 Composed of various domains : A1-A2-B-A3-C1-C2.
 Thrombin cleaves FVIII to form FVIIIa.
 This thn acts as a cofactor for FX to FXa.

Von willibrand factor
 High molecular weight component.
 Autosomal inheritance
 Synthesised by endothelial cells and megakaryocytes.
 Functions : carrier protein for FVIII and also mediates
adhesion of plts to subendothelium at sites of vessel
damage.

CHRISTMAS FACTOR
 Vit K Dependent.
 Activated by FXIa and FVIIa
 Inherited as sex linked manner
 Def: Hemophilia B

Stuart Prower factor
 Vit k dependent
 Activated by both intrinsic and extrinsic pathways.

FACTOR XII
 Site of production : Liver
 FXII to FXIIa by kalikerin , plasmin and by
autoactivation.
 Functions : prekalikerin to kalikerin
 Converts FXI to FXIa
 Activates fibrinolytic and complement systems.

FACTOR XIII
 It is a transglutaminase
 Stablizes fibrin clot.

HIGH MOLECULAR WEIGHT
KININOGEN
 Accelerates activation of FXII and prekalikerin.
 It is a source of bradykinin.
 Bradykinin : increases vessel permeability, small vessel
dilatation, smooth muscles contraction, vasodilation
,antithrombotic and antiplatelet activity.

FIBRINOLYTIC SYSTEM
 PROCESS OF DISSOLUTION OF BLOOD CLOTS IN
ORDER TO MAINTAIN BLOOD IN FLOW STATE.
 Major enzyme : plasmin
 Plasmin can cleave fibrinogen as well as fibrin.
 Plasmin digests insoluble-cross linked fibrin to release
FDP which are then cleared by macrophages.

 ACTIVATORS : tissue plasminogen activator and
kallikerin
 INHIBITORS : alpha-2 antiplasmin , alpha -2
macroglobulin , plasminogen activator inhibitors (PAI1
AND PAI 2) , thrombin activated fibrinolytic inhibitor
(TAFI).

NATURAL INHIBITORS OF
COAGULATION
 ANTITHROMBIN
 PROTEIN C
 PROTEIN S
 TISSUE FACTOR PATHWAY INHIBITOR (TFPI)

LABORATORY TEST FOR
SECONDARY HEMOSTASIS

SPECIMEN COLLECTION
 Venepuncture blood
 Anticoagulant of choice : 3.2% aq trisodium citrate.
 Blood : anticoagulant ratio = 9:1

Automatation in coagulation
 Nephelometry
 Electromechanical clot detection systems (steel ball)
 Chromogenic detection methods
 Thromboelastography
 Calliberated automated thrombogram
 Rotem

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Secondary hemostasis - coagulation cascades and lab tests

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Secondary hemostasis - coagulation cascades and lab tests