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.

Structure and composition

Platelets are small, circulating pieces, non-nucleated round or oval 2 – 4 μ in diameter. A

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

(Glycoproteins) lipids (phospholipids, cholesterol and glycolipids) Out of all glycoprotein

and phospholipids are functionally important plasma membrane contains glycoprotein

receptors.

Glycoproteins:

• Prevents the adherence of platelets to normal endothelium.

• Accelerates the adherence of platelets to collagen and damaged endothelium in

ruptured blood vessels.

• Forms a receptor for adenosine diphosphate (ADP) and thrombin.

2.Microtubule: Made up of tubulin (proteins)

• It responsible for the discoid shape of the platelets

3.Cytoplasm: cytoplasm are such active factors as

(1) actin and myosin molecules, which are contractile proteins similar to those found

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

and especially store large quantities of calcium ions.

(3) mitochondria and enzyme systems the power house of cell that are capable of

forming adenosine triphosphate (ATP) and adenosine diphosphate (ADP).

(4) enzyme systems that synthesize prostaglandins, which are local hormones that

cause many vascular and other local tissue reactions.

(5) an important protein called fibrin-stabilizing factor, helps in blood coagulation

(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

repair damaged vascular walls.

Properties
1. Adhesiveness-whenever comes in contact with any

wet or rough surface gets activated & stick to

surface. Factors responsible are – collagen,

thrombin, ADP, thromboxane A2, Ca ion & Von-

Willebrand Factor

2. Aggregation-property to stick to each other.

Factors responsible are ADP & Thromboxane A2

3. Agglutination-property of clumping together of

platelet. Its due to platelet Agglutinins. 

Functions
The functions of platelet are;

 Role in haemostasis.

 Role in clot formation.

 Role in clot retraction.

 Role in repair of injured blood vessels.

 Role in defence mechanism.

 Transport & storage function.

Role in haemostasis.

 Haemostasis – spontaneous arrest of bleeding from injured blood vessel.

 Vasoconstriction – by 5HT & other vasoconstrictors

 Temporary haemostatic plug – by platelets due to its property of adhesiveness &

aggregation.
  Definite haemostatic plug – also initiated by platelets.

Role in clot formation.

 Play important role in formation of intrinsic prothrombin activator

 It is responsible for onset of blood clotting.

Role in clot retraction.

 Contraction of contractile proteins i.e. Actin, Myosin & Thrombosthenin.

 Responsible for clot Retraction & wound healing.

Role in repair of injured blood vessels.

 Platelet derived growth factor (PDGF) in cytoplasm of platelet imp for Repair of

Endothelium.

Role in defence mechanism.

  Due to the property of agglutination, platelets are capable of Phagocytosis.

 Mainly in Phagocytosis of carbon particles, viruses & immune complexes.

Transport & storage function.

 Platelet when passes through GIT takes 5- HT against concentration gradient, stored

& transported to the site of injury.

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

2. Formation of the Platelet Plug

 3. Blood Coagulation

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

endothelial cells(endothelin) and platelets (5HT and other vasoconstrictors)

The contraction results from;

(1) local myogenic spasm,

(2) local autacoid factors from the traumatized tissues and blood platelets, and

(3) nervous reflexes.

The nervous reflexes are initiated by pain nerve impulses or other sensory impulses that

originate from the traumatized vessel or nearby tissues.

However, even more vasoconstriction probably results from local myogenic contraction of

the blood vessels initiated by direct damage to the vascular wall.

For the smaller vessels, the platelets are responsible for much of the vasoconstriction by

releasing a vasoconstrictor substance, thromboxane A2. The more severely a vessel is

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

can take place.

2. Formation of the Platelet Plug

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

by a blood clot. The process includes;

 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

 These chemicals are attracting the nearby platelets

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

 That’s why it’s called temporary haemostatic plug

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

Clotting Factor Synonyms

Factor I Fibrinogen
Factor II Prothrombin
Factor III Tissue factor; tissue thromboplastin
Factor IV Calcium
Factor V Proaccelerin; labile factor; Ac-globulin (Ac-G)
Factor VII Serum prothrombin conversion accelerator (SPCA); proconvertin; stable
factor
Factor VIII Antihemophilic factor (AHF); antihemophilic globulin (AHG);
antihemophilic factor A
Factor IX Plasma thromboplastin component (PTC); Christmas factor; antihemophilic
factor B
Factor X Stuart factor; Stuart-Power factor
Factor XI Plasma thromboplastin antecedent (PTA); antihemophilic factor C
Factor XII Hageman factor
Factor XIII Fibrin-stabilizing factor
Prekallikrein Fletcher factor
High-molecular- Fitzgerald factor; HMWK (high-molecular-weight kininogen)
weight kininogen Platelets

Mechanism of coagulation

The process of coagulation involves cascade of reactions

Activation of one factor leads to activation of next clotting factor

This enzyme cascade reaction is also called “Water Fall Sequence”

Steps in coagulation

Three main steps:

 Formation of prothrombin activator

 Conversion of prothrombin to thrombin

 Conversion of fibrinogen to fibrin

 Conversion of prothrombin to thrombin

Formation of prothrombin activator

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.

Conversion of fibrinogen to fibrin

It involves 3 reactions

 Proteolysis

 Polymerization

 Stabilization of fibrin polymers

Soluble fibrinogen

Proteolysis

Fibrin monomer

Polymerization

Fibrin polymer

(Soluble fibrin clot)

Stabilization of polymer

Insoluble fibrin clot

In this stage formation of covalent cross linkages between fibrin threads.

It adds tremendous strength to the fibrin meshwork.

This insoluble fibrin meshwork traps the remaining components of plasma and blood cells to

form a solid mass called clot

Blood clot retraction

 Within a few minutes after a clot is formed it begins to contract

 Platelets are essential for clot retraction

 The contractile proteins (actin, myosin, thrombosthenin) present in the cytoplasm of

platelets causing strong contraction.

4. Fibrinolysis

 It is a process that prevents blood clots from growing and becoming problematic.

 In fibrinolysis, a fibrin clot, the product of coagulation, is broken down.

 Its main enzyme plasmin cuts the fibrin mesh at various places

Fibrinolytic mechanisms

As soon as clot develops, another series of events take place locally.

Plasminogen adsorbed on the clot

Plasmin Breaks down fibrin threads

Fibrin threads are engulfed by reticulo -endothelial system

Factors affecting coagulation

Role of vitamin k – required for the synthesis of prothrombin, VII, IX and X by the liver.

Hence these factors are called vitamin k dependent pro-coagulants.

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

platelets. Also acts as a carrier of factor VIII.

Reference:

Hall, J. E. (2011). Pocket companion to Guyton and Hall textbook of medical physiology.

Saunders.