Primary and secondary Haemostasis

1. Dr Abhijith J Puttanani 1

2.  Haemostasis is a process that prevents bleeding at
the site of an injury while maintaining normal
blood flow elsewhere
 4 Major Steps
 Vasoconstriction
 Primary Haemostasis (platelet plug formation)
 Secondary Haemostasis (clot formation)
 Fibrinolysis 2

3.  Vessel's first response to injury
 Greater the trauma more will be the spasm ,sometimes it can occlude the vessels
completely
 Triggers
 Direct injury to vascular smooth muscle
 Secretion of nitric oxide, prostaglandins stop; secretion of endothelin begins → further contraction
 Nervous system reflexes initiated by local pain receptors.
 Effects
 Slows down the flow of blood via the vessel
 Increases the period of contact between platelets and exposed collagen
3

4.  Process by which a platelet plug is formed
 Steps
 1,Exposure
 Endothelial injury  Damage to endothelial cells
exposes collagen
 Damaged cells release Von Willebrand factor which
binds to the exposed collagen
4

5.  2,Adhesion
 GP1B surface proteins on platelets bind
to Von Willebrand factor
 Von Willebrand factor is a large
glycoprotein that is present in the
plasma and endothelium
 Once VWF binds to the subendothelium,
it exposes multiple binding sites for
platelets to adhere, activate, and
aggregate.
5

6. 6
 3, Activation
 Platelet changes shape ,first swells then contracts & forms arms to grab other
platelets, releases more von Willebrand factor, serotonin, calcium, ADP,
thromboxane A2 (positive feedback loop)
 ADP, thromboxane A2 result in GPIIB/IIIA expression

7. 7
 4,Aggregation
 GPIIB/IIIA binds to fibrinogen, links platelets → platelet plug

8.  Clinically
 Patient can be asymptomatic
 Skin bleeding – Petechiae , Purpura ,Ecchymoses
 Mucosal Bleeding – Epistaxis ,Gingival Bleeding, Menorrhagia, Haemoptysis
 Investigations
 Platelet Count
 Bleeding Time
 Platelet Aggregometry(Best Method)
8

9.  Aka Secondary Haemostasis.
 End product - fibrin meshwork.
 Its called a cascade as from one stage to the
next in the Cascade, a greater amount of
proenzyme is involved resulting in
amplification.
 Each factor is named in the order of their
discovery.
 Consists of three pathways, the extrinsic,
intrinsic, and common pathways, that interact
together to form a stable blood clot 9

10. 10
Intrinsic
Pathway
Extrinsic
Pathway
Common
Pathway
Stable Clot

11. 11
Intrinsic
Pathway
Extrinsic
Pathway
Common
Pathway
Stable Clot
The extrinsic and intrinsic coagulation pathways both lead into the final common
pathway by independently activating factor X.
X
Xa

12. 12
Thrombin
Prothrombin
Fibrinogen Fibrin
Xa
Va
Ca++
Membrane Phospholipids
STABLE FIBRIN
CLOT
X X

13. 13
Thrombin
Prothrombin
Fibrinogen Fibrin
Prothrombinase
Complex
STABLE FIBRIN
CLOT

14. 14
Thrombin
Prothrombin
Fibrinogen Fibrin
Xa
Va
Ca++
Membrane Phospholipids
STABLE FIBRIN
CLOT

15. 15
Thrombin
Prothrombin
Fibrinogen Fibrin
Xa
Va
Ca++
Membrane Phospholipids
STABLE FIBRIN
CLOT
X
V
Thrombin
XII
I
XIII
a
Ca++
Thrombin

16. 16
Thrombin
Prothrombin
Fibrinogen Fibrin
Xa
Va
Ca++
Membrane Phospholipids
STABLE FIBRIN
CLOT
X X

17. 17
X Xa

18. 18
X
X
a
• Intrinsic pathway begins when factor XII or the
Hageman factor is exposed to collagen,
kallikrein, and high molecular weight kininogen
(HMWK) and is subsequently activated.
• Factor XIIa activates factor XI into XIa.
• With a calcium ion, factor XIa activates factor
IX
• Then, factor IXa, factor VIIIa, and calcium form
a complex to activate factor X.
• Factor VIII is found in the blood and is often
activated by thrombin (factor IIa).
• aPTT measures both Intrinsic and Common

19. 19
Thrombin
Prothrombin
Fibrinogen Fibrin
Xa
Va
Ca++
Membrane Phospholipids
STABLE FIBRIN
CLOT
X X

20. 20
X
X
a *Tissue factor is aka tissue thromboplastin

21. 21
X Xa
• The extrinsic pathway begins when there is
injury to the surrounding tissues
• Which exposes tissue factor (factor III) to the
blood.
• Tissue factor then becomes bound with
calcium and factor VIIa to activate factor X
• Factor VII is present in the blood and
requires vitamin K to be activated.
• PT measures both Extrinsic and common
pathway

22. 22
Thrombin
Prothrombin
Fibrinogen Fibrin
Xa
Va
Ca++
Membrane Phospholipids
STABLE FIBRIN
CLOT
X X

23. 23
• Vitamin K regulates blood coagulation
converts coagulation factors into mature
forms
• Quinone reductase reduces vitamin K quinone
(dietary form) into vitamin K hydroquinone
• Vitamin K hydroquinone donates electrons to
y-glutamyl carboxylase,
• Which Activates the enzyme
• Adds carboxyl group to glutamic acid residues
on proteins
• This coverts the clotting factors to its active
form
• Vit K dependant Factors are
II, VII, IX, X

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