Thrombocytes (Platelets): Vascular spasm, Platelets plug formation, Coagulation (blood clotting)
Blood Platelets
Blood platelets are disc-shaped, non-nucleated cell fragments that range in diameter from 2 to 4 µm. In actuality, platelets are not cells. They come from fragments of the cytoplasm of megakaryocytes that live in the red bone marrow.
1. The granulomere, a central zone of platelets, contains calcium ions, ADP, ATP, serotonin, pyrophosphate, hydrolytic enzymes, P-selectin, fibrinogen, platelet-derived growth factor, coagulation factors V and XIII, and other substances.
2. Each platelet has a hyalomere, a transparent zone with a light blue stain on the periphery.
3. Under a light microscope, platelets look like clusters of cells due to their high stickiness. They also help in blood clotting and blood vessel wall repair, which stops blood loss.
4. The normal range for platelet counts in microliters of blood is 200,000–400,000,000. The thrombopoietin that the kidneys secrete can promote the production of platelets.
5. The lifespan of platelets is about ten days.
Haemostasis= Hemostasis
The Haemostasis Steps
1. Vascular spasm 2. Formation of platelet plugs 3. Blood clotting, or coagulation
Fibrynolysis
1. Vascular spasm Caused by:
A. Direct injury (vasoconstriction, particularly in the damaged area).
B. Chemicals (such as thromboxanes released by damaged vessels and serotonin generated by platelets that cluster on injured blood vessels).
1. Primary aggregation: platelets aggregate to reveal collagen after endothelial discontinuities. Therefore, the first step to stop bleeding is to produce a platelet block.
2. Secondary aggregation: ADP and a sticky glycoprotein are released by platelets in the plug. Both have strong platelet aggregation, which causes the platelet clog to enlarge.
3. Coagulation (blood clotting)
Blood coagulation is crucial for stopping bleeding from a damaged blood artery. Coagulation is a complicated process with numerous phases and components, the majority of which are proteins. Roman numerals I through XIII are used to identify the factors,
1. Prothrombin activator is created when these clotting factors activate one another in a particular order. The last common pathway of blood coagulation begins with the prothrombin activator.
2. The prothrombin activator transforms prothrombin, which is found in plasma, into thrombin, an enzyme, in the last common pathway.
3. Thrombin breaks down the plasma protein fibrinogen into insoluble fibrin fibres, which create a meshwork that entangles blood and causes a blood clot.
There are two mechanisms (pathways) that can start the last common pathway:
1. Tissue injury triggers the extrinsic route.
2. Endothelial cell injury triggers the intrinsic pathway. The following slides outline the various steps that make up each pathway.
Fibrinolysis
• Once the clot has formed, the injured blood vessel must be healed to remove it.
• The initial phase in the healing process is fibrinolysis or the disintegration of the clot.
• The plasmin is produced from plasminogen.
Plasmin is responsible for breaking down fibrin into soluble forms.
• The blood vessel wall’s integrity is restored as the clot is eliminated through the healing process.
Control of Coagulation
The body regulates and restricts the coagulation cascade to prevent the clotting process from spreading throughout the circulatory system once it has begun.
The primary controls are:
1. Normal blood artery endothelial cells are perfectly smooth, which prevents platelets from adhering to them.
2. The blood’s naturally occurring anticoagulants, such as heparin, which deactivate clotting factors.