Haemostasis is the physiological process of stopping bleeding from injured blood vessels. It involves three main processes: vasoconstriction of the injured vessel, formation of a temporary platelet plug, and formation of a definitive fibrin blood clot. Blood coagulation is initiated through the intrinsic and extrinsic pathways, ultimately activating thrombin which converts fibrinogen to fibrin to form a stable clot. Calcium ions and clotting factors I-XIII are required at various steps of coagulation. The liver plays a key role in synthesizing clotting factors and removing activated factors to maintain blood in a fluid state.

1. HAEMOSTASIS

2. HAEMOSTASIS
■
■
Definition – spontaneous arrest or stoppage of bleeding
from injured blood vessel by physiological process.
3 processes
■
■
■
Vasoconstriction
Formation of temporary haemostatic plug formation
Formation of Definitive haemostatic plug formation

3. Summary of reactions involved in
hemostasis

4. The Vascular and Platelet Phases of
Hemostasis

5. The Coagulation Phase of Hemostasis

6. The Coagulation Phase of Hemostasis

7. VASOCONSTRICTION

8. FORMATION OF TEMPORARY
HAEMOSTATIC PLUG FORMATION

9. PLATELET ADHESION

10. PLATELET ACTIVATION

11. PLATELET AGGREGATION

12. FORMATION OF TEMPORARY
HAEMOSTATIC PLUG

13. FORMATION OF DEFINITIVE
HAEMOSTATIC PLUG FORMATION
■ Temporary plug
converted to definitive
plug by Process of
blood coagulation.
■ Results in formation of
tight unyielding seal

14. COAGULATION OF BLOOD
■ Through out life blood – in
fluid state but when
removed or shed or
collected in container
become jelly like – clot
■ Fluidity – necessary for
circulation.
■ Coagulation – protect
from excessive bleeding.

15. CLOTTING FACTORS
■ I – FIBRINOGEN
■ Soluble
■ Mol wt – 3,40,000
Dalton
■ 6 polypeptide chain
■ Conc. – 0.3 gm/100 ml
■ It is converted into
fibrin in the presence of
enzyme thrombin

16. CLOTTING FACTORS
■ II- PROTHROMBIN
■ Inactive precursor of
thrombin.
■ Mol wt 69000 dalton.
■ Synthesized in liver in
the presence of vitamin
K.
■ Conc. is 40 mg / 100
ml.

17. CLOTTING FACTORS
■ III – THROMBOPLASTIN
■ Also called tissue factor or tissue thromboplastin
■ Released in extrinsic pathway.

18. CLOTTING FACTORS
■ IV – CALCIUM
■ Essential in all stages of coagulation.

19. CLOTTING FACTORS
■ V – LABILE FACTOR / PROACCLERIN
■ Required for formation of protrombin activator
■ Consumed during clotting so absent in serum.

20. CLOTTING FACTORS
■ VII – STABLE FACTOR / PROCONVERTIN
■ For activation of factor X in extrinsic pathway.

21. CLOTTING FACTORS
■ VIII – ANTI-HAEMOPHYLLIC FACTOR A / ANTI-
HAEMOPHLIC GLOBULIN.
■ Protein of b globulin type, synthesized in liver.
■ Activation of factor x
■ Deficiency causes classical Haemophilia.
■ Inherited disease in which CT prolonged.

22. CLOTTING FACTORS
■ IX – ANTI-HAEMOPHILIC FACTOR B/ PLASMA
THROMBOPLASTIC COMPONENT
■ First discovered in patient named Christmas.

23. CLOTTING FACTORS
■ X –STUART-PROWER FACTOR
■ Along with active factor V, Ca and phopholipid forms a
complex – Prothrombin activator.
■ Formed in both extrinsic & intrinsic pathway.

24. CLOTTING FACTORS
■ XI – PLASMA THROMBOPLASTIN
ANTICEDENT / ANTI-HAEMOPHILIC FACTOR C
■ Its deficiency causes hemorrhagic state.

25. CLOTTING FACTORS
■ XII – HAGEMAN FACTOR/ GLASS FACTOR /
CONTACT FACTOR
■ Activated when comes in contact with electronegative
surface or glass or rough surface.
■ Its activation initiate intrinsic pathway.

26. CLOTTING FACTORS
■ XIII – FIBRIN STABILIZING FACTOR /
FIBRINASE / LAKI LORAND FACTOR
■ Required for activation of fibrin polymer along with Ca.

27. Special attributes of process of
coagulation
1. There is enzyme substrate reaction
2. The system acts as a bio amplifier system.
3. There is cascade reaction.
4. Ca++ are essential in almost all steps.

28. BLOOD COAGULATION
• Intrinsic pathway Extrinsic pathway
Prothrombin activator complex
XIII
Prothrombin Thrombin
XIIIa
Fibrinogen Fibrin (monomer)
Fibrin(polymer) Fibrin clot

29. Coagulation of blood
Intrinsic pathway: When the blood is exposed to
• Damaged endothelial cells or
• Collagen fibers underlying the endothelium
• Trauma to the blood itself
• Electro negatively charged wettable surfaces such as
glass (In vitro)
Extrinsic pathway
• Begins with the release of tissue thromboplastin from
the traumatized vascular wall or extravascular tissue

30. Intrinsic pathway
Endothelial damage + Collagen exposure
XII XIIa
XI XIa
IX IXa
X Xa
Prothrombin activator
Platelets
Phospholipids
Ca
VIIIa, Ca
HMW Kininogen, Plasma kallikrein
VIII
V Va, Ca

31. Extrinsic pathway
Tissue thromboplastin
VII VIIa
X Xa
Phospholipids, Ca, III
Prothrombin activator
Va,Ca
V

33. MECHANISM OF COAGULATION-
INTRINSIC PATHWAY.

34. EXTRINSIC PATHWAY.

35. THROMBIN.
▪Proteolytic enzyme.
▪Amount of thrombin produced during
clotting of 1 ml of blood is sufficient to
coagulate 3 liters of blood.

36. FIBRINOGEN TO FIBRIN.
■ Proteolysis
■ Polymerization .
■ Stabilization of fibrin polymers.

37. BLOOD CLOT RETRACTION.
■ Clot is meshwork of fibrin with entrapped blood
cells , platelets & plasma.
■ Contractile proteins – Actin, myosin &
thrombosthenin.
■ Compress fibrin meshwork squeeze out serum.
■ Clot reduced to 40% of original volume.

38. ROLE OF CALCIUM.
■ Except for first 2 steps Ca required for all steps.
■ Ca removal causes Anticoagulation.
■ e.g. use of oxalates & citrates.

39. ROLE OF VITAMIN K.
Chemical structure.
■ Fat soluble , insoluble in water.
Sources.
■ Food , bacterial flora.
Role of vitamin K
■ Synthesis of coagulants like Prothrombin.
■ Factor VII , IX & X & circulatory anticoagulant
protein.

40. ROLE OF LIVER.
■ Synthesis of procoagulants – site of synthesis of
factor V,VII,IX,X, Prothrombin & fibrinogen
■ Removal of activated procoagulants.
■ Synthesis of anticoagulants like – heparin, anti
thrombin III & protein C

41. BLOOD IN FLUID STATE
■ Velocity of circulation.
■ Surface effect of endothelium.
■ Glycocalyx
■ Circulatory anticoagulants.
■ Fibrinolytic mechanism.
■ Removal of activated clotting factors.

42. CIRCULATORY ANTICOAGULANTS.
■ Natural anti-coagulant.
■ Heparin
■ Antithrombin-III
■ Alpha 2 macroglobulin
■ Protein C

43. FIBRINOLYTIC MECHANISM.
■ Protein C
■ Inactivates inhibitor of
TPA
■ Increases Plasmin
formation
■ Acts as Fibrinolytic

44. REMOVAL OF ACTIVATED CLOTTING
FACTORS.
■ Liver plays an important role
■ Removes activated clotting factors
■ Prevents Intravascular Clotting

45. THROMBOSIS
■ Def.– Intravascular
clotting of blood & clot so
formed is thrombus
■ Thrombus – Def – Solid
mass formed in the
living heart or blood
vessel from the
constituents of blood.

46. THROMBOSIS
■ Virchow’s triad
which predisposes to
thrombus formation.
■ Predisposing factors
■ Endothelial injury
■ Alteration of blood flow
■ Hypercoagulability of
blood

47. PREVENTION OF THROMBI
■ – decrease platelet adhesion; Aspirin, Dextran
■ Anticoagulants – Heparin, Dicoumarol
■ Intermittent compression or electrical
stimulation of calf muscle
s