Platelets PDF

# Platelets Platelets are the smallest of all blood cells and form a creamy white layer on top of the white cells after Centrifugation. They are round oval or nid Shaped about 1.5 Um in diameter, bound by a membrane and Packed with granules, but with no nucleus. ## Maintainance of shape by Microtu...

# Platelets Platelets are the smallest of all blood cells and form a creamy white layer on top of the white cells after Centrifugation. They are round oval or nid Shaped about 1.5 Um in diameter, bound by a membrane and Packed with granules, but with no nucleus. ## Maintainance of shape by Microtubules The shape of platelet cell is maintained by a ring of microtubules at the Periphery; Hive call membrane is much folded and there is an extensive tubular system in the Cytoplasm which Communicates with plasma. ## Membrane Receptors on the membrane of platelet cells are receptors which are glycoproteins. The receptors are for collagen, for exogenous activators and for von willebrand factor of the vessel wall, Which promote platelet adhesion both to the vessel wall and to one another during haemostasis. ## Contractile proteins (thrombosthenin) The cytoplasm Contains a contractile protein known as thrombostherin made up of two fragments: - Thrombosthenin-M which resembles myasin - Thrombosthenin - A which resembles actin Contraction of the thrombasthenin enables the platelets to change Shape when ADP is present, aggregate, and cause clot retraction. ## Cytoplasmic Granules Platelets have a variety of granules which when secreted, play an important part in all phases of haemostasis namely, Vasoconstriction, platelet adhesion and aggregation to form the platelet plug, factors invaved in Coagulation and the healing of the wound in the blood vessel. This granules are of three types: 1. Alpha granules 2. Dense granules 3. Lysosomes ### Alpha granules contain: - factor v - fibrinogen - thrombaspondin - von willebrand factor - Platelet-derived growth factor ### Dense granules contain: - ADP - Serotonin - Calcium ### Lysosomes: - Hydrolytic enzymes active at low PH ## Origin of platelets Platelets Originate from fragmentation of megakaryocytes which in turn originate from the pluripotent stem cells in the marrow that give rise to all blood cells. ## Development of platelets The stages in the development of platelets are: - Megakaryoblast - pro-megakaryocyte - Megakaryocyte - Platelet (maturation is indicated by reduplication of nuclear maternal The cytoplasm matures by an increase in granularity and loss of Basophilia.) Platelets are formed from megakaryocytes by either of two processes: 1. Cytoplasmic pseudopodia which penetrate the wall of the manorw Sinusoids and are broken off isto the blood stream 2. Baj vesicle formation throughout the cytoplasm which fuse and fragment the cytoplasm intis platelets, leaving the nucleus to degenerate ## Functions of platelets The functions of platelets is in the arrest of bleeding through: - platelet plug which block the damaged small blood vessels - secretion of various substances which are important in blood coagulation and clot retractior; ## Normal Valves The normal range IS 200-400 ×10³/µl with a mean of about 250 ×103/μι ## Lifespan of platelet The lifespan of platelets in the blood Circulation, estimated by The use of chromium labelling, is 9-12 days ## Destruction off platelets Damaged or old platelets are: phagocytused by macrophages of the Mononuclear -phagocyte systrin especially in the spleen ## Regulation of thrombopases The number of platelets in the blood Circulation of an individual is fairly constant, indicating theit the rate of production is rega-lated to match the rate of platelet destruction or disappearance: The mechanism is not clear but some colony stimulating factors (thrombopoietin). ## Platelet Disorders A bleeding tendency maybe due to decrease in the number of platelets (thrombocytopenia) or a defect in the function. ## Thrombocytopenia how platelet counts maybe due to any of the three mechanisms: 1. failure of maturation of meyakaryocytes which may occur in marrow hypoplasia, idiopathic or thug-induced, and marrow infiltration with cancer cells 2. increased Consumption of platelets or used up due to disseminated intravascular coagulation, HIV and Epstein Barr virus and bacterial infection 3. Excessive destruction of platelets by abnormal large spleen, this is seen in chronic malaria, portal hypertension 2.t.c ## Platelet Functron Disorder The cause may be due to: 1. Defective adhesion due to low or absent von Willebrand factor or absence of von willelorand receptors 2. Defective aggregation. Anti-inflammatory drigs such as aspirin Inhibit the synthesis of pletelets 3. Defective release reaction of which aspirin is the commonert Cause.