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Lec.6 November 13,2017Prof. Dr.Baybeen Al-selevany

Platelets or thrombocytes

Objectives Structure Normal Count Life span Thrombopoiesis Functions Hameostasis'

Platelets are referred to as thrombocytes because of their sealing function i.e. they form a thrombus, or plug, when there is a break in the circulatory system.Are about 40 times more common than leukocytes in the blood.

Structure Platelets do not have nuclei .Platelets are discoid-shaped packages of cytoplasm surround by a membrane. Platelets surface has many openings that extended deeply into the interior of the structure which give the platelets a sponglike appearance. Clotting factors such as factor I (fibrinogen), factor V (labile factor) & factor VIII (antihemophilic factor A) are adhere to these openings.. Also the membrane contain large amount of phospholipids [(platelet factor 3(PF3)] which plays an important role in clotting process. The platelet cytoplasm contains large quantities of ADP, ATP, serotonin, Ca++ & thromboxanes A2, factor XIII &, actin & myosin (that can cause contraction of the platelet these contractile proteins are important in clot retraction).

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Normal count the normal concentration of platelet in the blood is 200,000 – 500,000 platelets/c.mm. Average value is 300,000/c.mm (1ml). Thrombocytopenia: is a condition in which the platelet count is greatly reduced. While thrombocytosis.

Life span: is 5 – 9 days.

Thrombopoiesis: is the process of platelet production or development: All platelets are divided from cells in bone marrow called megakaryoblasts, The maturation of megakaryocytes is regulated by growth factor called thrombopoietin.

Functions Platelets form the second major component of the haemostatic system. Platelets have several functions, all of which are related to haemeostasis

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(prevention of blood loss). Platelets play an important role in preventing blood loss in the following ways:1.Blood loss from intact blood vessel is preventing by the structure of the endothelial cells that form the vessel walls. Endothelial cells lined the inner surface of blood vessels & are attached to the collagen fibers in the connective tissues of blood vessel .Endothelial cells form tight junction and prevent loss of blood cells & plasma proteins from the circulation. Platelets are required to maintain the structural integrity of the vessel walls. When endothelial cells separate in the intact blood vessels, platelets fill small gaps that may have occurred thus prevent the loss of blood cells & plasma from the circulation. When the number of platelets is reduced (i.e. thrombocytopenia), the gaps appear between the cells & blood leaks out of blood vessels into the tissues .So Platelets play a role in keeping endothelial cells in good shape.

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2.The formation of platelet plugs, that seal holes in damaged blood vessel walls as a result of vessel injury, is known as the primary haemostatic plug .formation & it greatly limits the loss of blood from the circulation. 3.The formation of clots, which help seal off larger wounds in the vessels. This process of haemostasis is called secondary haemostasis.

Haemostasis means arrest of bleeding which is very important to the maintenance of homeostasis. If not stopped excessive bleeding from a cut or torn blood vessel can result in a positive feedback pathway, consisting of decreasing blood volume & blood pressure & resulting in death. Haemostasis can be divided into two types:1. Primary haemostasis. 2. Secondary haemostasis Primary haemostasis: occurs in minor skin wounds. It’s subdivided into: 1. Vascular spasm (vasoconstriction). 2. A temporary haemostatic plug of platelets.Vascular spasm: Local vasoconstriction is an immediate but temporary closure of a blood vessel resulting from contraction of smooth muscle within the wall of the blood vessel, which reduces the flow of blood from the vessel rupture. Local vasoconstriction is caused by chemical mediators such as endothelin released from damaged blood vessels, thromboxane A2 is the most potent vasoconstrictor released by the platelets at the site of injury, and serotonin from aggregating platelets. Vascular spasm (constriction) is a transient process, usually lasting less than a minute. However this amount of time is sufficient for plug formation by platelet to start.Platelets plug formation: a platelet plug: is an accumulation of platelets that can seal up small breaks in blood vessel. Platelets plug formation is very important in maintaining the integrity of the circulatory system because tears occur in the smaller vessels & capillaries many times each day, and platelet plug formation quickly closes them. People who lack the normal number of platelets tend to develop numerous small hemorrhages

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in their skin & internal organs. The steps of the primary haemostatic plug formation are:Step I: platelet adhesion occurs when platelets bind to exposed collagen fibers of endothelial damaged blood vessel. This adhesion requires certain essential coagulation factor such as Von willebrand factor which is secreted by blood vessel endothelial cells. This factor is a part of complex clotting factor VIII (8). Step II: activation of platelets by collagen cause release of ADP, thromboxane A2 (derivative of prostaglandins) which are in turn activated additional plateletsStep III:, a plasma protein fibrinogen will bind platelets together resulting in the formation of a platelet plug which seal the wound and prevent bleeding but this plug is temporary stops within few 2 – 6 minutes which is called bleeding time. Step IV: Activated platelets express phospholipids & coagulation factor V (labile factor), which are important part of clot formation.

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The clot (fibrin) plugs the hole in the blood vessel until the endothelial repaired. This stable plug is temporary. The clot (fibrin) is gradually degraded by a series of enzymes also present in the blood. In minor skin wounds bleeding stops within a few minutes.

Clinical NoteThe production of prostaglandins and thromboxan A2 are very important for platelet plug formation as is demonstrated by the effect of aspirin. Because aspirin inhibits prostaglandin synthesis & the production of thromboxanes resulting in reduced platelet activation. If an expectant mother ingests large quantities of aspirin near the end of pregnancy, synthesis of thromboxane A2 is inhibited & several effects are possible. The infant, mother, or both may die as a result of hemorrhage. On the other hand in a stroke (cerebral infarction) or heart attack (myocardial infarction), platelet plugs and clots can form in vessels & threaten the life of the individual. Small amounts of aspirin daily can help prevent such vascular problems. Aspirin is a drug that inhibits platelet activity i.e. anti -platelet drug.