Platelets-Composition, Function, Hemostasis and Its Individual Phases
Platelets-Composition, Function, Hemostasis and Its Individual Phases
Platelets-Composition, Function, Hemostasis and Its Individual Phases
Platelet
Platelets is formally known as thrombocytes, which are not whole cells but rather fragments
or pieces of cells.
normal platelet count is1,50,000 – 3,50,000/mm³ life span average 8 days. Thrombopoietin is
a hormone produced by the liver that increases the rate of platelet production.
Microscopic picture:
1.Cell membrane
2.Microtubule
3.Cytoplasm
1.Cell Membrane: It is 6 nm thick and contain Carbohydrates(glycocalyx), Proteins
receptors.
Glycoproteins:
in muscle cells, and still another contractile protein, thrombosthenin, that can cause the
platelets to contract.
(2) endoplasmic reticulum and the Golgi apparatus that synthesize various enzymes
(3) mitochondria and enzyme systems the power house of cell that are capable of
(4) enzyme systems that synthesize prostaglandins, which are local hormones that
(6) a growth factor that causes vascular endothelial cells, vascular smooth muscle
cells, and fibroblasts to multiply and grow, thus causing cellular growth that eventually helps
Willebrand Factor
Functions
The functions of platelet are;
Role in haemostasis.
Role in haemostasis.
aggregation.
Definite haemostatic plug – also initiated by platelets.
Platelet derived growth factor (PDGF) in cytoplasm of platelet imp for Repair of
Endothelium.
Platelet when passes through GIT takes 5- HT against concentration gradient, stored
Hemostasis
Heme = blood; stasis = to halt
It is the process of forming clots in the wall of damaged blood vessels & preventing blood
loss while maintaining blood in a fluid state with in the vascular system.
Stages of Hemostasis
1. Vascular Constriction
4. Fibrinolysis
1. Vascular Constriction
It is the first response to injury. It reduces the amount of blood flow in damaged areas and
limits the amount of blood loss. These responses are triggered by some chemicals released by
(2) local autacoid factors from the traumatized tissues and blood platelets, and
The nervous reflexes are initiated by pain nerve impulses or other sensory impulses that
However, even more vasoconstriction probably results from local myogenic contraction of
For the smaller vessels, the platelets are responsible for much of the vasoconstriction by
traumatized, the greater the degree of vascular spasm. The spasm can last for many minutes
or even hours, during which time the processes of platelet plugging and blood coagulation
If the cut in the blood vessel is very small—indeed, many very small vascular holes do
develop throughout the body each day—the cut is often sealed by a platelet plug, rather than
Platelet Adhesion
Platelet Activation
Platelet Aggregation
Platelet Adhesion
Following vascular constriction platelets become sticky and adhere to the collagen
matrix in sub-endothelium.
Platelet Activation
After platelets adhere to the collagen fibres it become spiked and much stickier.
Platelets released large quantity of ADP and thromboxane A2 from its storage
granules
Platelet Aggregation
Large number of activated platelets stick to each other and forming platelet aggregation
or platelet plug.
Platelet plug is fairly loose but it successful in blocking the blood loss
3. Blood Coagulation
Blood remains in fluid condition within the blood vessels throughout life. But when the blood
is shed from the blood vessels or collected in a container, it loses it fluidity within a few
minutes and gets converted into jelly-like mass, which is called” clot”. This phenomenon is
called coagulation.
Clotting factors
Mechanism of coagulation
Steps in coagulation
Intrinsic pathway
Extrinsic pathway
Conversion of prothrombin to thrombin
Prothrombin activator
Prothrombin Thrombin
Ca2+
This process is caused by the prothrombin activator in the presence of ca2+ . This occurs at
the surface of platelets which form the platelet plug at the site of injury.
It involves 3 reactions
Proteolysis
Polymerization
Soluble fibrinogen
Proteolysis
Fibrin monomer
Polymerization
Fibrin polymer
Stabilization of polymer
This insoluble fibrin meshwork traps the remaining components of plasma and blood cells to
It is a process that prevents blood clots from growing and becoming problematic.
Its main enzyme plasmin cuts the fibrin mesh at various places
Fibrinolytic mechanisms
Role of vitamin k – required for the synthesis of prothrombin, VII, IX and X by the liver.
Role of liver – liver synthesizes pro-coagulants like prothrombin, fibrinogen, factors V, VII
IX, X XI.
Role of blood vessels – releases substances like plasminogen activators, tissue factors, von
-Willebrand factor.
Role of von- Willebrand factor – acts as a bridge between denuded vascular endothelium and
Reference:
Saunders.