Hemostasis is the process by which bleeding is stopped. It involves three main mechanisms: 1. Vasoconstriction of blood vessels to reduce blood flow through the damaged vessel. 2. Formation of a platelet plug at the site of injury through platelet adhesion, activation, and aggregation. Chemicals released by platelets attract more platelets to form a temporary plug. 3. Coagulation cascade where prothrombin is converted to thrombin which then converts fibrinogen to fibrin, forming a mesh that strengthens the platelet plug. Over time fibrin is broken down by plasmin in a process called fibrinolysis to remove the clot from the blood vessel. Together these processes

2. HAEMOSTASIS AND
PLATELET PLUG
FORMATION
Faiz Sajid Khan
Roll Number: 36
FY-BDS: 2018

3. Blood And It’s Contents
■ Blood is a specialized fluid connective tissue comprising of 55% fluid plasma and 45%
formed elements.
■ Plasma (55%) is a straw colored clear liquid part of blood. It contains 91-92% of water
and 8-9% of solids. Plasma contains ions, water, proteins, nutrients, wastes and
gases.
■ The 45% formed elements comprises of Erythrocytes (RBC’s) , Leukocytes (WBC’s)
and Thrombocytes (Platelets).

4. Blood performs various functions involving
transport of respiratory gases, nutrients;
excretion of waste products of metabolism;
maintaining homeostasis of the body; plays
a major role in defense mechanism of the
body and performs Hemostasis.
This presentation deals with the most
important function of blood i.e. Hemostasis.
Objectives:
1. Definition of Hemostasis.
2. Mechanism of Hemostasis
3. Platelet Plug Formation In detail.
4. Homeostasis VS Hemostasis.

5. Definition Of Hemostasis
■ The term hemostasis means prevention of blood loss.
■ It is a process which causes bleeding to stop, meaning to keep blood within a
damaged blood vessel. It is the first stage of wound healing. This involves
coagulation, blood changing from a liquid to a gel.
Hemostasis depends on the integration of three
elements that will produce three mechanisms to
achieve hemostasis:
1. Vasoconstriction or Vascular Spasm.
2. Formation of Platelet Plug.
3. Coagulation cascade.
4. Fibrinolysis.

6. Step 1: Vascular Spasm or Vasoconstriction
■ Injury at any site of the body.
■ Blood vessels cut, the endothelium is damaged and the collagen is exposed.
■ Arterioles and arteries constrict, reducing the blood loss.
■ Platelet activation takes place by adherence of platelets to the exposed collagen fibers.
■ Secretion of Serotonin (Vasoconstrictor) which causes constriction of blood vessels,
preventing further blood loss.
■ Adherence of platelets to the collagen stimulated by Von Willebrand factor.

7. Role Of Serotonin & Von Willebrand
Factor
1. Serotonin: Serotonin is transported by platelets and
released upon activation. This induces constriction of
injured blood vessels and enhances platelet
aggregation to minimize blood loss. Recent studies
have shown that activation of platelet serotonin
induces shedding of important adhesion molecules. As
a consequence, platelets lose their ability to contribute
to thrombus formation.
2. Von Willebrand Factor: Von Willebrand Factors,
primary function is binding to other proteins, in
particular factor VIII, and it is important in platelet
adhesion to wound sites. It is not an enzyme hence has
no catalytic activity.

8. Step 2: Platelet Plug
Formation
■ At the site of vessel injury, platelets stick
together to create a plug, which is the
beginning of blood clot formation.
■ The second critical step in haemostasis, which
follows vasoconstriction, is platelet plug
formation.
The three steps to platelet plug formation are-
1. Platelet adherence.
2. Platelet activation.
3. Platelet aggregation

9. 1. Platelet Adherence: Following vascular spasm, platelets become sticky and
adhere to the collagen matrix in sub endothelium.
2. Platelet Activation: After Platelets adhere to the collagen fibers, they become
spiked and much stickier. Platelets release large quantity of ADP and Thromboxane
A2 from its storage granules. These chemicals attract nearby platelet molecules and
activate them.
3. Platelet Aggregation: All these Platelets aggregate together and form a loose
temporary platelet plug, which closes the injured part of the vessel and prevents
further blood loss. The platelet aggregation is accelerated by Platelet Activating
Factor. (PAF)

10. Step 3: Coagulation Cascade
■ In general blood coagulation occurs in three stages:
1. Formation of Prothrombin Activator- Blood clotting commences with the formation of a
substance called prothrombin activator whose formation is initiated by substances produces
either within the blood or outside the blood.
2. Conversion of Prothrombin into Thrombin-
Calcium

11. 3. Conversion Of Fibrinogen into Fibrin-
Thrombin
Fibrin Stabilizing Factor VIII
Step 4: Fibrinolysis
■ The lysis of the blood clot inside the blood vessel is called fibrinolysis. It helps to
remove the clot from the lumen of the blood vessel.
■ Requires a substance called Plasmin or Fibrinolysin.

13. Haemo-Dictionary
Thrombin: Serine protease that
converts fibrinogen into fibrin.
Functions as a procoagulant and
Anticoagulant. It is a agonist for a
number of cellular responses
during inflammation and wound
repair.
Platelet Activating Factor (PAF): It is a
potent phospholipid activator and
mediator of many leukocyte
functions, platelet aggregation and
degranulation, inflammation etc. Also
involved in changes to vascular
permeability.
Thromboxane A2: Produced by
activated platelets and has
prothrombin like properties:
Stimulates activation of new platelets
as well as increases platelet
aggregation.
Plasmin: Formed from inactivated
glycoprotein called plasminogen.
Plasminogen is synthesized in liver
and converted into plasmin by tissue
plasminogen activator, lysosomal
enzymes and thrombin. Causes lysis of
clot by dissolving and digesting the
fibrin threads.

16. Hemostasis VS Homeostasis