INTRODUCTION TO

HAEMOSTASIS
 Objectives
• Define haemostasis
• Overview of the coagulation cascade
• Coagulation factors and their common
names
• Common routine tests in coagulation
 What is HAEMOSTASIS?
• It is the cessation of blood loss from a
damaged vessel. It is the process by
which blood clot is formed through a
series of event in the blood.
• A thrombus is an intravascular clot formed
during life
 Haemostasis contd
• Blood vessel (vascular wall)
• Platelets
• Coagulation factors
• Plasma proteins
 Process of Haemostasis
• Vascular Spasm - The smooth muscle in blood vessel
walls contracts immediately the blood vessel is broken.
This response reduces blood loss for some time, while
the other hemostatic mechanisms become active.

• Platelet Plug Formation - When blood platelets

encounter a damaged blood vessel they form a "platelet
plug" to help to close the gap in the broken blood vessel.

• Blood Clotting (Coagulation)

• Dissolution of Clot by Plasmin (Fibrinolysis)

 Platelet Kinetics
• Platelets are produced in blood cell formation (thrombopoiesis) in bone
marrow, by budding off from megakaryocytes.
• The physiological range for platelets is 150-400 x 109 per litre.
• Around 1 x 1011 platelets are produced each day by an average adult.
• The lifespan of circulating platelets is 7-10 days.
• This process is regulated by thrombopoietin, a hormone usually produced by
the liver and kidney.
• Each megakaryocyte produces between 5,000 and 10,000 platelets.
• Old platelets are destroyed by the spleen and by Kupffer cells in the liver
Platelet Structure
Platelet Structure contd
Platelet Glycoproteins (GPs) or
Receptors
• GP Ia – Adhesion to collagen
• GP Ib –Adhesion of von willebrand factor
• GP IIb/IIIa (fibrinogen receptor) –platelet-
platelet aggregation
 Formation of primary
haemostatic plug
• Platelet activation
• Shape change
• Platelet release reaction (granule
secretion)
• Synthesis of Thromboxane A2
• Platelet adhesion
• Platelet aggregation
 What is Coagulation cascade ?
• Coagulation is initiated almost instantly after an injury to
the blood vessel damages the endothelium (lining of the
vessel). Platelets immediately form a hemostatic plug at
the site of injury; this is called primary hemostasis.
Secondary hemostasis occurs simultaneously—proteins in
the blood plasma, called coagulation factors, respond in a
complex cascade to form fibrin strands which strengthen
the platelet plug
• Biological amplification system which is initiated by tissue
damage or vascular injury, with resultant sequential
activation of coagulation factors in which thrombin is
generated.
Coagulation cascade
Coagulation cascade
 Coagulation factors and their
common names
• Factor I - fibrinogen
• Factor II - prothrombin
• Factor III - tissue thromboplastin (tissue factor)
• Factor IV - ionized calcium ( Ca++ )
• Factor V - labile factor or proaccelerin
• Factor VI - unassigned
• Factor VII - stable factor or proconvertin
• Factor VIII - antihemophilic factor
• Factor IX - plasma thromboplastin component, Christmas factor
• Factor X - Stuart-Prower factor
• Factor XI - plasma thromboplastin antecedent
• Factor XII - Hageman factor
• Factor XIII - fibrin-stabilizing factor
 Fibrinolysis
• Tissue plasminogen activator released
from ECs activates plasminogen;
• Plasminogen is converted to plasmin
• Plasmin breaks down Fibrin into fibrin
degradation products (FDPs)
Inhibitors of coagulation factors
• Tissue factor pathway inhibitor inhibits
VIIa and extrinsic pathway
• Antithrombin inhibits IIa, IXa, XIIa, XIa, Xa
• Proteins C and S inhibits Va and VIIIa
• Tissue plasminogen activator inhibitor
(tPAI)-inhibits fibrinolysis
 Common routine tests in
coagulation
• Prothrombin time (PT)
• Activated partial thromboplastin time
(aPTT)
• Thrombin time (TT)
• Fibrinogen quantitation
• Factor assays
 SUMMARY
• Haemostasis is an important mechanism in
controlling blood loss
• Coagulation cascade includes the extrinsic,
intrinsic and common pathway
• Coagulation Factors and their common
names
• Inhibitors of coagulation provide protective
mechanisms for unchecked blood
coagulation