The Roles of Platelets

1. Primary aggregation. Platelets in the damaged region attach to collagen revealed by the discontinuity in the vessel wall, forming a platelet plug.

2. Secondary aggregation. Platelets in the plug release the contents of their alpha and delta granules. This release of serotonin explains the higher concentration of serotonin in serum than in plasma. Scrotonin, a vasoconstrictor, restricts blood flow to the damaged area by causing contraction of vascular smooth muscle.

3. Blood coagulation. Platelets release fibrinogen in addition to that normally found in the plasma. The fibrinogen is converted by the clotting factor cascade into fibrin, which forms a dense fibrous mat to which more platelets and other blood cells attach, forming a clot and plugging the opening in the blood vessel wall.

D. Clot Retraction: The clot initially bulges into the vessel lumen, but later it contracts and condenses through the interactions of thromhosthenin and platelet actin, myosin, and ATP.

E. Clot Removal: As the vessel wall heals and the protection afforded by the clot is no longer needed, the clot is removed by the enzyme plasmin, Plasmin is formed by the action of plasminogen activators on the plasma proenzyme plasminogen Enzymes released by the lambda granules (lysosomes) of the platelets also aid in clot digestion

CLOT FORMATION - Blood clotting

A. The Clot and Serum: Clotted blood consists of 2 parts:

(1) the clot, or thrombus, which includes the formed elements and some of the proteins previously dissolved in the plasma, and

(2) the serum, a clear yellow liquid that is similar to plasma except that it lacks fibrinogen and contains more serotonin.

B. Clotting Factors: Clotting involves a cascade of molecular interactions among several plasma proteins and ions (clotting factors I-XIII). The cascade can be initiated by 2 converging pathways, each of which results in the conversion of fibrinogen to fibrin by the enzyme thrombin. In the intrinsic pathway, initiation of the cascade occurs when factor XII is activated by contact with collagen underlying the endothelium (indicating damage to the endothelial lining of a vessel). In the extrinsic pathway, cells in a damaged vessel wall or the surrounding tissue release an ill-defined clot-promoting substance termed thromboplastin (factor III), which com bines with blood calcium and factor VII to activate factor X, a plasma protein. Factor X is a point of convergence of the 2 pathways and, in its activated form, promotes the conversion of prothrombin (factor II) to thrombin. Both factor X and prothrombin are synthesized by the liver and require vitamin K as a cofactor in their synthesis. Thrombin enzymatically converts plasma fibrinogen (factor I, released into plasma by platelets and by the liver) into fibrin; this explains the lower concentration of fibrinogen in serum than in plasma. Other factors act as promoters and accelerators of the clotting process or help stabilize the fibrin once it has formed. An inherited abnormality in factor VIII (whose precise role in the clotting process is uncertain) results in the clotting disorder known as hemophilia.

Blood Platelets

Platelets, or thrombocytes, the smallest formed elements in the blood histology , are disklike cell fragments that vary in diameter from 2 to 5 um. In humans, they lack nuclei and originate by budding from large cells in the bone marrow called megakaryocytes. They range in number from 200,000 to 400,000 mm3 of blood and have a lifespan of about 8 days. In blood smears they appear in clumps. Each platelet has a peripheral hyalomere region that stains a faint blue and a dense central granulomere that contains a few mitochondria and glycogen granules and a variety of purple granules. Platelets have an important physical role in plugging wounds, and they contribute to the cascade of molecular interactions among the various clotting factors dissolved in the plasma blood histology


Basophils are the least numerous of the circulating leukocytcs, constituting 1% of the white blood cells of healthy adults. Like other white blood cells, basophils may leave the circulation, but they are capable of only very limited ameboid movement and phagocytosis in the tissues. Extravascular basophils are found most often at sites of inflammation and may be the major cell type at sites of cutaneous basophil hypersensitivity. Despite structural and functional similarities between basophils and mast cells, these cells are not the same and are distinguishable on the basis of ultrastructure. blood histology