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- Dr. E. R. Venkata Subba Reddy
Blood coagulation is part of an important

  host defense mechanism termed
  hemostasis.
 Hemostasis : arrest or stoppage of bleeding
  from a blood vessel.
 Injury to a blood vessel initiates a series of
  reactions resulting in hemostasis.
 Three stages : 1. Vasoconstriction
                 2. Formation of platelet plug
                 3. Coagulation of blood
Injury to blood vessel
                          ↓
                Endothelial damage and
                 collagen exposure

VonWillebrand factor →   I
                         ↓
              Activation of platelets          FIBRINOGEN
               ↓                 ↓                   I
         Serotonin             ADP +                 I
               I              TX A2                  I
               I                 ↓                    I
               I            Aggregation of            I
                            more platelets
               I                                      I
               I                 ↓                   ↓
         Vasoconstriction      platelet plug     FIBRIN (clot)
          (STAGE 1)             (STAGE 2)          (STAGE 3)
Definition : The process in which blood

  looses its fluidity and becomes a jelly
  like mass few minutes after its shed out or
  collected in a container.
 The so formed mass is called clot
 The clot is a mesh of thin fibrils
  entangling the blood cells .These fibrils
  consist of fibrin. The fibrin is formed from
  fibrinogen.
ENZYME CASCADE THEORY

- Factors in inactive proenzyme forms
- Series of proenzyme-enzyme conversions
  ( Zymogen activation reactions )
- At each stage a precursor protein
   (zymogen) is converted to an active
   protease by cleavage of one or more
   peptide bonds
- Helped by cofactors, calcium
3 STAGES



1. Formation of Prothrombin Activator
2. Conversion of Prothrombin to Thrombin
3. Conversion of Fibrinogen to Fibrin
Two ways

1. Contact activation pathway (formerly
 known as the intrinsic pathway)
2. Tissue factor pathway
  (extrinsic pathway)
Endothelial damage               +   collagen exposure
        I Kallikrein &                            I
       ↓ HMW kinogen                              I
XII ------XIIa                                    ↓
                  HMW kinogen                 Platelets
           ↓
   XI ------XIa                                     I
                     Calcium                        I
              ↓
   IX ------------ IXa                               ↓
                         VIII & Ca           Phospholipid
                    ↓
       X------------------ Xa                       I
                    I                                I
                    ↓                              ↓

           PROTHROMBIN ACTIVATOR ( PTA )
             (Xa + V + Ca +Phospholipid)
Tissue trauma + Tissue thromboplastin
                         ↓
                 Glycoprotein
                 Phospholipid
                       I
VII --------------------------------- VIIa
                       I      Ca
                       ↓      Phospholipid

 X ----------------------------------- Xa
                     I       Ca
                     I       Factor V
                     I       Thrombin
                     ↓

      Prothrombin activator
   (Xa + V + Ca +phospholipid)
PROTHROMBIN ACTIVATOR
               I
               ↓
  PROTHROMBIN-----------------→THROMBIN
                                     I
                                     ↓
      FIBRINOGEN a ←------------------------- FIBRINOGEN
                 I
  Polymerization I
                 ↓             XIII & Ca
LOOSE STRANDS OF FIBRIN-------------------------------→FIBRIN
                                        TIGHT BLOOD CLOT
The substances necessary for clotting are

    called clotting factors
    Thirteen identified



I – Fibrinogen
II – Prothrombin
III – Thromboplastin
IV – Calcium
V – Labile factor ( proaccelerin )
VI – presence not proved
VII – Stable factor
VIII – Anti hemophilic factor
IX – Christmas factor
X – Stuart-Prower factor
XI – Plasma Thromboplastin antecedent
XII – Hageman factor
XIII – Fibrin stabilizing factor (Fibrinase)
Calcium

 Phospholipid
 Vitamin K is an essential factor to a
  hepatic gamma-glutamyl carboxylase
  that adds a carboxyl group to glutamic
  acid residues on factors II, VII, IX and X,
  as well as protein S, Protein C and
  protein Z.
Five mechanisms keep platelet activation and the

    coagulation cascade in check.

    Protein C is a major physiological anticoagulant.

      It is a vitamin K-dependent serine protease .
    Activated by thrombin with the help of
    thrombomodulin.
      The activated form, along with protein S and a
    phospholipid as cofactors, degrades Va and VIIIa.

    Antithrombin is a serine protease inhibitor

    Tissue pathway factor inhibitor(TFPI)

    Plasmin cleaves fibrin into fibrin degradation products

    that inhibit excessive fibrin formation.
    Prostacyclin (PGI2) through cAMP inhibits platelet

    activation
Clot consists of entrapped platelets,

  RBCs, WBCs within the fibrin meshwork.
 Clot Retraction : after 30 to 45 min.
  -Clot contracts. Serum oozes out.
  -Actin, myosin and Thrombosthenin.
 FIBRINOLYSIS : lysis in blood vessel.
  Requires plasmin (fibrinolysin)
Commonly used:

    aPTT ( activated partial Thromboplastin time) - The

    contact factor pathway
    PT (also used to determine INR)- The tissue factor

    pathway
    Fibrinogen testing (often by the Clauss method)

    Platelet count

    Platelet function testing (often by PFA-100).

Others: Thrombin clotting time, Bleeding

    time, Mixing test (whether an
    abnormality corrects if the patient's
    plasma is mixed with normal
    plasma), Coagulation factor
    assays, Antiphospholipid antibodies, D-
    dimer, Genetic tests (factor V
    leiden), Miscellaneous platelet function
    tests, Thromboelastography (TEG or
    ROTEM), Euglobulin lysis test(ELT), .
Platelet disorders:

-Inborn or Acquired
-congenital:
> Glanzmann’s thrombasthenia - It is
   characterized by a defect in GPIIb/IIIa
   fibrinogen receptor complex,
 > Bernard-sourlier syndrome (abnormal
   glycoprotein Ib-IX-V complex),
 > Gray platelet syndrome(deficient α-granules),
 > Delta storage pool deficiency(deficient dense
   granules).
-Acquired: MDS, ITP, TTP, HUS, PNH, DIC, HIT.
HAEMOPHILIA: 3 main forms

- Hemophilia A : VIII deficiency
- Hemophilia B : IX
- Hemophilia C : XI
 Von Willebrand disease : most common
  hereditary bleeding disorder . Def of
  vWF, that mediates glycoprotein Ib
  (GPIb) binding to collagen.
Thrombosis is the pathological

  development of blood clots. May form an
  embolus or cause occlusionocclusion by
  embolus or thrombus leads to ischemic
  necrosis of tissue.
 Most cases of thrombosis are due to
  acquired extrinsic problems
  (surgery, cancer, immobility, obesity,)
 A small proportion of people harbor
  predisposing conditions known collectively
  as Thrombophilia (antiphospholipid
  syndrome, factor V leiden).
Adsorbent chemicals, such as zeolites, used for

    use in sealing severe injuries quickly (traumatic
    bleeding secondary to gunshot wounds).
    Thrombin and fibrin glue are used surgically to

    treat bleeding and to thrombose aneurysms.
    Desmopressin is used to improve platelet function

    Prothrombin complex concentrate,

    cryoprecipitate and fresh frozen plasma
    Recoombinant activated human factor VII is

    increasingly popular in the treatment of major
    bleeding.
    Tranexemic acid and aminocaproic acid inhibit

    fibrinolysis.
Anticoagulants and anti-platelets.

    Anti platelet agents : aspirin, clopidogrel, dipyridamole

    and ticlopidine; the parenteral glycoprotein Iib/IIIa
    inhibitors are used during angioplasty
    Anticoagulants, Warfarin (and related coumarins) and

    Heparin are the most commonly used.
    Warfarin affects the vitamin K-dependent clotting factors

    (II, VII, IX,X).
    Heparin and related compounds increase the action of

    antithrombin on thrombin and factor Xa.
     A newer class of drugs, the direct thrombin inhibitors, is

    under development; some members are already in clinical
    use (such as lepirudin).
    compounds that interfere directly with the enzymatic

    action of particular coagulation factors (e.g.,
    rivaroxaban).
--- Thankyou

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  • 1. - Dr. E. R. Venkata Subba Reddy
  • 2. Blood coagulation is part of an important  host defense mechanism termed hemostasis.  Hemostasis : arrest or stoppage of bleeding from a blood vessel.  Injury to a blood vessel initiates a series of reactions resulting in hemostasis.  Three stages : 1. Vasoconstriction 2. Formation of platelet plug 3. Coagulation of blood
  • 3. Injury to blood vessel ↓ Endothelial damage and collagen exposure VonWillebrand factor → I ↓ Activation of platelets FIBRINOGEN ↓ ↓ I Serotonin ADP + I I TX A2 I I ↓ I I Aggregation of I more platelets I I I ↓ ↓ Vasoconstriction platelet plug FIBRIN (clot) (STAGE 1) (STAGE 2) (STAGE 3)
  • 4. Definition : The process in which blood  looses its fluidity and becomes a jelly like mass few minutes after its shed out or collected in a container.  The so formed mass is called clot  The clot is a mesh of thin fibrils entangling the blood cells .These fibrils consist of fibrin. The fibrin is formed from fibrinogen.
  • 5. ENZYME CASCADE THEORY  - Factors in inactive proenzyme forms - Series of proenzyme-enzyme conversions ( Zymogen activation reactions ) - At each stage a precursor protein (zymogen) is converted to an active protease by cleavage of one or more peptide bonds - Helped by cofactors, calcium
  • 6. 3 STAGES  1. Formation of Prothrombin Activator 2. Conversion of Prothrombin to Thrombin 3. Conversion of Fibrinogen to Fibrin
  • 7. Two ways  1. Contact activation pathway (formerly known as the intrinsic pathway) 2. Tissue factor pathway (extrinsic pathway)
  • 8. Endothelial damage + collagen exposure I Kallikrein & I ↓ HMW kinogen I XII ------XIIa ↓ HMW kinogen Platelets ↓ XI ------XIa I Calcium I ↓ IX ------------ IXa ↓ VIII & Ca Phospholipid ↓ X------------------ Xa I I I ↓ ↓ PROTHROMBIN ACTIVATOR ( PTA ) (Xa + V + Ca +Phospholipid)
  • 9. Tissue trauma + Tissue thromboplastin ↓ Glycoprotein Phospholipid I VII --------------------------------- VIIa I Ca ↓ Phospholipid X ----------------------------------- Xa I Ca I Factor V I Thrombin ↓ Prothrombin activator (Xa + V + Ca +phospholipid)
  • 10. PROTHROMBIN ACTIVATOR I ↓ PROTHROMBIN-----------------→THROMBIN I ↓ FIBRINOGEN a ←------------------------- FIBRINOGEN I Polymerization I ↓ XIII & Ca LOOSE STRANDS OF FIBRIN-------------------------------→FIBRIN TIGHT BLOOD CLOT
  • 11. The substances necessary for clotting are  called clotting factors Thirteen identified  I – Fibrinogen II – Prothrombin III – Thromboplastin IV – Calcium V – Labile factor ( proaccelerin ) VI – presence not proved VII – Stable factor
  • 12. VIII – Anti hemophilic factor IX – Christmas factor X – Stuart-Prower factor XI – Plasma Thromboplastin antecedent XII – Hageman factor XIII – Fibrin stabilizing factor (Fibrinase)
  • 13. Calcium   Phospholipid  Vitamin K is an essential factor to a hepatic gamma-glutamyl carboxylase that adds a carboxyl group to glutamic acid residues on factors II, VII, IX and X, as well as protein S, Protein C and protein Z.
  • 14. Five mechanisms keep platelet activation and the  coagulation cascade in check. Protein C is a major physiological anticoagulant.  It is a vitamin K-dependent serine protease . Activated by thrombin with the help of thrombomodulin. The activated form, along with protein S and a phospholipid as cofactors, degrades Va and VIIIa. Antithrombin is a serine protease inhibitor  Tissue pathway factor inhibitor(TFPI)  Plasmin cleaves fibrin into fibrin degradation products  that inhibit excessive fibrin formation. Prostacyclin (PGI2) through cAMP inhibits platelet  activation
  • 15. Clot consists of entrapped platelets,  RBCs, WBCs within the fibrin meshwork.  Clot Retraction : after 30 to 45 min. -Clot contracts. Serum oozes out. -Actin, myosin and Thrombosthenin.  FIBRINOLYSIS : lysis in blood vessel. Requires plasmin (fibrinolysin)
  • 16. Commonly used: aPTT ( activated partial Thromboplastin time) - The  contact factor pathway PT (also used to determine INR)- The tissue factor  pathway Fibrinogen testing (often by the Clauss method)  Platelet count  Platelet function testing (often by PFA-100). 
  • 17. Others: Thrombin clotting time, Bleeding  time, Mixing test (whether an abnormality corrects if the patient's plasma is mixed with normal plasma), Coagulation factor assays, Antiphospholipid antibodies, D- dimer, Genetic tests (factor V leiden), Miscellaneous platelet function tests, Thromboelastography (TEG or ROTEM), Euglobulin lysis test(ELT), .
  • 18. Platelet disorders:  -Inborn or Acquired -congenital: > Glanzmann’s thrombasthenia - It is characterized by a defect in GPIIb/IIIa fibrinogen receptor complex, > Bernard-sourlier syndrome (abnormal glycoprotein Ib-IX-V complex), > Gray platelet syndrome(deficient α-granules), > Delta storage pool deficiency(deficient dense granules). -Acquired: MDS, ITP, TTP, HUS, PNH, DIC, HIT.
  • 19. HAEMOPHILIA: 3 main forms  - Hemophilia A : VIII deficiency - Hemophilia B : IX - Hemophilia C : XI  Von Willebrand disease : most common hereditary bleeding disorder . Def of vWF, that mediates glycoprotein Ib (GPIb) binding to collagen.
  • 20. Thrombosis is the pathological  development of blood clots. May form an embolus or cause occlusionocclusion by embolus or thrombus leads to ischemic necrosis of tissue.  Most cases of thrombosis are due to acquired extrinsic problems (surgery, cancer, immobility, obesity,)  A small proportion of people harbor predisposing conditions known collectively as Thrombophilia (antiphospholipid syndrome, factor V leiden).
  • 21. Adsorbent chemicals, such as zeolites, used for  use in sealing severe injuries quickly (traumatic bleeding secondary to gunshot wounds). Thrombin and fibrin glue are used surgically to  treat bleeding and to thrombose aneurysms. Desmopressin is used to improve platelet function  Prothrombin complex concentrate,  cryoprecipitate and fresh frozen plasma Recoombinant activated human factor VII is  increasingly popular in the treatment of major bleeding. Tranexemic acid and aminocaproic acid inhibit  fibrinolysis.
  • 22. Anticoagulants and anti-platelets.  Anti platelet agents : aspirin, clopidogrel, dipyridamole  and ticlopidine; the parenteral glycoprotein Iib/IIIa inhibitors are used during angioplasty Anticoagulants, Warfarin (and related coumarins) and  Heparin are the most commonly used. Warfarin affects the vitamin K-dependent clotting factors  (II, VII, IX,X). Heparin and related compounds increase the action of  antithrombin on thrombin and factor Xa. A newer class of drugs, the direct thrombin inhibitors, is  under development; some members are already in clinical use (such as lepirudin). compounds that interfere directly with the enzymatic  action of particular coagulation factors (e.g., rivaroxaban).