Platelets|Thrombocytes|Purpura|

                                         

                Platelets|Thrombocytes| Thrombasthenia|Purpura

This article discusses different aspects of platelets. Learn about the expected levels of platelets, indications, and more.

Keywords: Thrombocytosis| Thrombocytopenia |Thrombosthenia| Bernerd Soulier syndrome| Thrombocytophoresis| Haemostatic|

Table of contents
1.	Introduction
2.	Discovery
3.	Normal life span
4.	Average count
4.	Structure
5.	Functions

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Introduction:

Thrombocytes or platelets are colorless spherical oval or rod-shaped bodies. The average size of platelets is 2-4 microns in diameter. They are very complex specialized cells without a nucleus capable of responding quickly and precisely to various activators, e.g., A.D.P., Calcium ions, etc.

Discovery

George Gulliver, 1841, drew a picture of Platelets.

William Addison, in 1842, drew a picture of the platelet-fibrin clot.

Lionel Beal 1864 published a sketch of Platelets.

Dr.Richard Hill Noris described the action of Platelets in 1880.

James Wright examined blood smears using the Wright stain named after him and used the term Plates in his 1906 publication but changed it to Platelet in his 1910 publication, a universally accepted term.

Thrombocytes were first used in the early 1900s and are sometimes used as synonyms for Platelets, but not generally in the scientific literature.

 

Platelets and R.B.C.

Life span

The life span of the Platelet is 8-12 days.

Structure

Their cytoplasm contains different types of granules. They are::

    1 . alpha granules–contain some protein and a variety of coagulation factors, fibrinogen, vWF, and PDGF-(Platelet-derived growth factor).

2. delta granules are dense and contain non-protein substances of low

 molecular weight like  ATP, Serotonin, and calcium.

3. lambda granules – They are lysosomes,that contain  acid hydrolases and hydrolytic enzymes.

When platelets are activated, the contents of these granules are discharged, promoting platelet aggregation and fibrin deposition on the Platelet.

Formation

Megakaryocytes produce them. Megakaryocytes are the largest (35-160 microns in diameter) in bone marrow, with irregular rings of lobed nuclei and granular cytoplasm. In the cytoplasm, microvesicles are formed, which will join to form a platelet.

Platelets are formed due to division in the cytoplasm and nucleus. Megakaryocyte dies, and platelets are released into the circulation. Several thousand platelets are removed from one megakaryocyte.

Platelets remain in the spleen for a short period before going into circulation.

The normal count

The average count is 1.5 to 4 lac per cubic millimeter of blood. The count is usually constant in health. There is some regulatory feedback mechanism to control its count. Like erythropoietin, it is assumed that thrombopoietin is present to regulate platelet formation

 but its presence is not confirmed.

 Platelet count is done by complete blood count (C.B.C.) and may be counted individually.

An average bleeding time reflects sufficient platelet number, functions, and normal microvasculature.

The average value  of bleeding time is -1 to 3 minutes 

Variation in the count

Thrombocytosis is when the platelet count is more than 4  lac per cubic millimeter of blood. It is  also known as thrombocythemia, which may be :

a)     A). Primary –a malignant proliferation of megakaryocytes. Cell count is higher in the primary type, but their functions are abnormal. Which is of two types :

                    1). Thrombocytosis when the only platelet count is raised.

2). Polycythemia rubra vera:  When all blood cells (R.B.C., WBC, and Platelets) count increases.

B). Secondary –it is a widespread form of Thrombocytosis. In this condition, only the platelet count and its normal functions are raised.

Thrombocytopenia is when the platelet count is less than 1.5 lac per cubic millimeter of blood.

Thrombasthenia

Thrombasthenia with abnormal functions when the platelet count is within the standard limit.

Spontaneous bleeding may take place. Transfusion of platelets is performed to prevent bleeding.

Thrombasthenia may be due to

Congenital disability of the -

1). Membrane glycoproteins –Bernerd Soulier syndrome.

2). Deficiency of dense granules.

Acquired :

Some drugs inhibit platelet functions. For example, aspirin, indomethacin, and other nonsteroidal anti-inflammatory drugs (NSAIDs) prevent cyclooxygenase, thus preventing the conversion of  Arachidonic acid to thromboxane B2.

Antibiotics, e.g., Penicillins, Heparin, and beta-blockers, also prevent platelet functions.

Thrombocytophoresis is the removal of platelets from circulation and is done in 

Thrombocytosis.

Site of Destruction

Platelets are destroyed in the reticuloendothelial system, mainly in the spleen. Therefore, platelets disappear from circulation in hypersplenism due to their rapid destruction.

Functions

1. The primary function is to form a hemostatic plug and maintain the integrity of vasculature.

2. Clot retraction by contraction of thrombosthenin- the actomyosin-like contractile protein in the platelets.

3. Phagocytosis of carbon particles, viruses, immune complexes, etc.

4. Storage and transport: of 5-HT, Histamin, etc.

Hashtags :Thrombocytosis# Thrombocytopenia #Thrombosthenia#Bernerd Soulier syndrome#Thrombocytophoresis#Haemostatic#

Internal link: https://blog.totalphysiology.com/2020/12/blood-composition-component-of-  blood.html

External link

    www.oneblood.org>media>blog

    www.pathkindlabs.com>blog

    www.thrombolux.com>blog

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