Platelets
They are not cells but small fragments of megakaryocyte cytoplasm. Platelets
are about 2-4 µm in diameter and possess lysosomes, endoplasmic reticulum, a
Golgi complex and Golgi vesicles or granules that contain a variety of factors
involved in platelet function. Platelets have pseudopods and are capable of
amoeboid movement and phagocytosis. The platelet count for normal individuals
ranges from 150000 - 400000 platelets/1mm³ (average about 250000/ 1mm³) of
blood.
Function of platelets:
1. They secrete vasoconstrictors(Thromboxane A2) that cause vascular spasm
in injured vessels.
2. Temporary Hemostasis-They form temporary platelet plugs to stop
bleeding.
3. Blood coagulation -( Platelet Phospholipids, platelet factor 4, and
synthesizing clotting factor V and XI
4. Clot retraction(contraction of Actin , Myosin & Thrombosthenin)
5. Thrombolysis:- They dissolve blood clots that have out-lasted their
usefulness.
6. Phagocytosis
7. Storage and transport
8. Vascular growth:-Platelets help in growth of vascular endothelium by
secreting platelet–derived growth factor (PDGF)- stimulate mitosis in
fibroblasts and smooth muscles, and help to maintain the lining of blood
vessels
Hemostasis:
It is a process of Arrest of bleeding (preventing blood loss). It includes:-
1. vascular spasm
2. Platelets plug formation
3. Clot formation ( coagulation)
4. Clot retraction
5. Clot dissolution
6. Growth of fibrous tissue into the blood clot to close the whole vessel
permanently.
Platelets play an important role in all above processes.
1. Vascular Spasm or Vasoconstriction:
When a blood vessel has been cut or ruptured (damaged), vascular
contraction (spasm) occurs, this contraction increases the resistance to
blood flow that minimize blood flow and reduces the loss of blood from
ruptured vessel. The contraction results from:-
- Local myogenic contraction of the blood vessel due to direct damage to
the vessel wall
- Local nervous reflexes
- Local humoral factors from the traumatized tissue
- Platelets from the smaller vessels are responsible for most of the vascular
constriction by releasing vasoconstricting substances like serotonin,
epinephrine and thromboxane A2
The local vascular spasm can last for many minutes and maintained long
enough, during which time, the processes of platelet plugging and blood clotting
can take place. People who lack the normal number of platelets tend to develop
numerous small hemorrhages in their skin and internal organs.
Figure (1): The Vascular Spasm Phase of the Hemostasis
2. Platelet Plug Formation:
This process can be described as series of steps, many of these events occur
simultaneously:-
Figure (2): Aggregation of Platelets at Site of Injury and Formation of Platelet Plug
a. Platelets Adhesion:
This step involves the binding of platelets to the exposed collagen of
the damaged vessel through a key protein which is Von Willibrand
factor (VWF). This protein is secreted by megakaryocytes, platelets
and endothelial cells lining the blood vessel. VWF binds to platelets
surface receptors and collagen, causing the platelets to adhere to
collagen while other platelets can bind directly to the collagen.
b. Platelets Activation:
Platelets adhere to collagen by VWF become activated. This activation
stimulates the platelets to secrete certain substances like Adenosine
diphosphate (ADP) and thromboxane which will result in further
activation of other platelets. Also, activated platelets secrete serotonin
and epinephrine which cause vasoconstriction.
c. Platelets Aggregation:
As platelets become activated, ADP stimulates morphological changes
in the platelets causing them to express surface receptors that can bind
to fibrinogen (a plasma protein). In platelets aggregation, the
fibrinogen forms a bridge between the surface receptors of different
platelets resulting in the formation of platelets plug. ADP stimulates
the production of thromboxane A2 (TXA2) which supports further
platelets aggregation.
d. Activated platelets express phospholipids (platelet factor III) and
coagulation factor V which are important part of clot formation.
Figure (2): The Process of Platelet Plug Formation
3. Clot Formation (Coagulation):
Vascular spasm and platelets plug alone are not sufficient to close large cuts.
A blood clot is a network of threadlike protein fibers called fibrin that
traps blood cells, platelets and fluid. Formation of blood clot depends on
a number of plasma proteins called coagulation factors, which normally are
present in inactive form and do not cause clotting.
Give Reason:
Platelet count is less in dengue Fever
Bleeding time can still be prolonged inspite of normal Platelet count