Haemostasis involves three components that work together to stop bleeding after an injury. The extravascular component involves pressure from accumulated blood in tissues around blood vessels. The vascular component involves constriction of blood vessels. The intravascular component involves platelets, coagulation factors, anticoagulants, and fibrinolytic factors that form a thrombus (blood clot) at the site of injury through a balance of pro-coagulant and anticoagulant processes. Disruptions to this balance can result in bleeding disorders or hypercoagulability.

1. HAEMOSTASIS
PRESENTED BY
MISS TASMIA ZEB

2. HAEMOSTASIS
• Haemostasis literally means “stoppage of blood flow”. There are three
basic components of haemostasis: extravascular, vascular and
intravascular. The extravascular component is mainly the pressure
exerted on the blood vessels because of accumulation of extravasated
blood in the tissue space. The efficiency of this component depends
upon the bulk of surrounding tissue, the type of tissue and the tone
of tissue. The vascular component constitutes the blood vessels
themselves. The role played by the blood vessels depends upon their
size, the amount of smooth muscle in their wall and the integrity of
the lining

3. HAEMOSTASIS
• endothelium. On injury the blood vessel undergoes vasoconstriction as a
neurogenic response thus decreasing the blood flow. Together with
extravascular component it may stop the blood flow altogether. The injury
exposes collagen and tissue factor that initiate the participation of
intravascular components of haemostasis. The key components in
intravascular haemostasis are the platelets, the coagulation factors,
anticoagulants and fibrinolytic factors. Platelets and coagulation factors
promote formation of thrombus, which occludes the injured site, and result in
arrest of bleeding. Anticoagulant proteins help in limiting the thrombus
formation to the site of injury whereas fibrinolytic factors help in dissolution
of the thrombus. A fine balance between these keeps the blood in fluid state.
• A tilt of the balance to one or other side may result in failure of coagulation
leading to a bleeding disorder or increased propensity to coagulation leading
to Hypercoagulable State or thrombosis.

4. • Exposure of collagen in the wall of blood vessel, following injury, provides surface for adhesion of
platelets. The platelets that adhere to this surface undergo metamorphosis and a release reaction,
which attracts more platelets leading to aggregation of platelets resulting in the formation of a
platelet plug. Numbers as well as functional integrity of platelets affect this phase in haemostasis.
This primary platelet plug is strengthened by the formation of fibrin threads and is converted into a
thrombus. Fibrin formation is initiated in two ways. First the injury to vessel wall leads to exposure
of tissue factor (TF) or factor III with which combines a plasma protein, factor VII, and initiates
extrinsic pathway of coagulation. The exposure of negatively charged elements of the vessel wall
(collagen) activates another protein, factor XII, which initiates the intrinsic pathway of coagulation.
The two pathways converge on a common pathway, activating factor X that, in turn complexes with
activated factor V. This complex converts prothrombin in the plasma into thrombin, which then
polymerise fibrinogen in the plasma to fibrin threads. These threads are then stabalised by the
action of activated factor XIII. In this cascade platelets also play a part by providing phospholipid.
The details are shown in Figure 33.26. In all, there are 12 proteins and one metal ion (Ca++), which
participate in coagulation process. These can be divided into three groups with similar properties.

5. GROUPS
• 1. Contact group: This includes Prekallikrein, High Molecular Weight
Kininogen (HMWK), factor XII and factor XI. These are activated on
exposure to negatively charged surfaces. These are also involved in
fibrinolysis and complement system. The site of their synthesis, apart
from factor XI that is synthesised in liver, is not clear. These are all
serine proteases.
• 2. Prothrombin group: This group includes factors II, VII, IX and X.
These are all serine proteases and are synthesised in liver. These
require vitamin K for γ carboxylation of glutamic acid residues to
convert these into pro-enzymes.
• 3. Fibrinogen group: This group includes factors I, V, VIII and XIII. Of
these I, V and XIII are synthesised in liver.

6. DISORDERS OF HAEMOSTASIS
• DISORDERS OF HAEMOSTASIS
Based on the physiology of haemostasis described above, the
disorders of haemostasis can be grouped into those arising because of:
1. Vascular defects
2. Platelet defects
3. Defects in coagulation pathway
4. Defects in anticoagulant pathway
5. Defects in fibrinolytic pathway
6. Others

7. BLOOD CLOTTING FACTORS
• 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

8. COAGULATION PATHWAYS
Coagulation can be initiated by either of two distinct pathways.
• The Intrinsic pathway can be initiated by events that take place
within the lumen of blood vessels. The Intrinsic pathway requires only
elements (clotting factors, Ca++, platelet surface etc.) found within, or
intrinsic to the vascular system.
• The Extrinsic pathway is the other route to coagulation. It requires
Tissue Factor (tissue thromboplastin), a substance which is "extrinsic
to", or not normally circulating in the vessel. Tissue Factor is released
when the vessel wall is ruptured.