This document summarizes the process of hemostasis, which involves stopping bleeding from damaged blood vessels. It occurs in three main steps: 1) Vasoconstriction, where the blood vessel constricts to reduce blood flow. 2) Formation of a temporary platelet plug at the site of injury through platelet adhesion, activation, and aggregation. 3) Formation of a definitive clot through the blood coagulation process, where the temporary platelet plug is converted into a tight blood clot to seal the damaged vessel. Platelets play a key role in both the temporary plug and activating the coagulation cascade to form the definitive clot.

1. HEMOSTASIS
SHARFUNNISA.S.H.
I M.SC. HN
&
AZMATHULLAH
I M.Sc.MGMD

2. INTRODUCTION
• Hemostasis combines the
terms “hemo” (meaning
“blood”) and “stasis” (meaning
“standing still”).
• Haemostasis refers to the
spontaneous arrest or
prevention of bleeding from
the injured/damaged vessels
by the physiological process

3. STEPS
Hemostasis involves three main
steps
• Vasoconstriction,
• Formation of temporary
haemostatic plug and
• Formation of the definitive
haemostatic clot.

4. 1. VASOCONSTRICTION
• Immediately after injury, the blood vessel
constrict and decreases the loss of blood from
the damaged portion
• When the blood vessel is cut ,the endothelial is
damaged and the collagen is exposed.
• Platelets adhere to this collagen and get
activated and produces vasoconstrictor
• Initial vasoconstriction is caused by direct effect
of injury on the vascular smooth muscles. The
initial vasoconstriction is transient but is
maintained for several minutes or even hours
by humoral facilitation due to release 5HT (5-
hydroxytryptamine) (serotonin) and other
vasoconstrictors.

5. 2. PLATELET PLUG FORMATION
Formation of a temporary haemostatic plug by the platelets at
the site of injury involves following steps:
• Platelet adhesions
• Platelet activation
• Platelet aggregation

6. PLATELET ADHESION
• Following injury, platelets come in contact
with the damaged collagen fibres and
endothelial cells of the vessel wall and
change their characteristics.
• That is, they begin to swell and assume
irregular forms with large number of
pseudopodia protruding from the surface.
• The contractile proteins of the platelets
contract forcibly and cause release of
granules that contain multiple factors.
• They become sticky and therefore adhere
to the collagen of damaged cell wall and to
the damaged endothelium.
Aspirin prevents platelet aggregation by inhibiting formation of
thromboxane A2. Therefore, aspirin in low doses is of value in
preventing myocardial infarction.

7. PLATELET ACTIVATION
• The platelets secrete large
quantities of ADP and
thromboxane A2, which act on the
nearby platelets and cause their
activation.
• Stickiness of these additional
platelets causes them to adhere to
originally activated platelets.
• In this way, a vicious cycle is
initiated which leads to activation
and adherence of large number of
platelets.

8. PLATELET AGGREGATION
• The large numbers of activated
sticky platelets stick to each other
forming platelets aggregation.
• Platelets aggregation is also
increased by platelet
activatingfactor, a cytokine secreted
by neutrophils, monocytes and
platelet cell membrane lipids.
• Platelet aggregation initiates a
series of reactions which result in
formation of thromboxane A2 and
prostacyclin from the platelet
membrane phospholipids.

9. FORMATION OF TEMPORARY HEMOSTATIC
PLUG
• The platelets adherence and aggregation
ultimately lead to the formation of platelet
plug.
• At first, it is a fairly loose plug but is
successful in blocking the blood loss if the
vascular opening is small.
• Inhibition of further plug formation:
Prostacyclin formed from the membrane
phospholipids inhibits thromboxane
formation and thus curtail the process of
further plug formation. This reaction
keeps the platelets plug localized, i.e.
prevents intravascular spread of plug.

10. FORMATION OF DEFINITIVE HAEMOSTATIC
PLUG
• The temporary platelet plug is converted
into the definitive haemostatic plug by the
process of clot formation (blood
coagulation) which involves a complex
series of events.
• Platelets play an important role in the
formation of the intrinsic prothrombin
activator which is responsible for initiating
the process of clot formation.
• Note. The blood clot formed at the site of
injury results in a tight unyielding seal or
the so-called definitive haemostatic plug.

12. THANK YOU