In case of injury, platelets, together with the coagulation cascade, form the first line of defense by forming a blood clot. Thus, hemostasis and host defense were intertwined in evolution. For example, in the Atlantic horseshoe crab (living fossil estimated to be over 400 million years old), the only blood cell type, the amebocyte, facilitates both the hemostatic function and the encapsulation and phagocytosis of pathogens by means of exocytosis of intracellular granules containing bactericidal defense molecules. Blood clotting supports the immune function by trapping the pathogenic bacteria within.Although thrombosis, blood coagulation in intact blood vessels, is usually viewed as a pathological immune response, leading to obturation of lumen of blood vessel and subsequent hypoxic tissue damage, in some cases, directed thrombosis, called immunothrombosis, can locally control the spread of the infection. The thrombosis is directed in concordance of platelets, neutrophils and monocytes. The process is initiated either by immune cells by activating their pattern recognition receptors (PRRs), or by platelet-bacterial binding. Platelets can bind to bacteria either directly through thrombocytic PRRs and bacterial surface proteins, or via plasma proteins that bind both to platelets and bacteria. Monocytes respond to bacterial pathogen-associated molecular patterns (PAMPs), or damage-associated molecular patterns (DAMPs) by activating the extrinsic pathway of coagulation. Neutrophils facilitate the blood coagulation by NETosis. In turn, the platelets facilitate neutrophils NETosis. NETs bind tissue factor, binding the coagulation centres to the location of infection. They also activate the intrinsic coagulation pathway by providing its negatively charged surface to the factor XII.
)One can get a clue as to whether bleeding is due to a platelet disorder or a coagulation factor disorder by the characteristics and location of the bleeding. : 815, Table 39-4  All of the following suggest platelet bleeding, not coagulation bleeding: the bleeding from a skin cut such as a razor nick is prompt and excessive, but can be controlled by pressure; spontaneous bleeding into the skin which causes a purplish stain named by its size: petechiae, purpura, ecchymoses; bleeding into mucous membranes causing bleeding gums, nose bleed, and gastrointestinal bleeding; menorrhagia; and intraretinal and intracranial bleeding. Excessive numbers of platelets, and/or normal platelets responding to abnormal vessel walls, can result in venous thrombosis and arterial thrombosis. The symptoms depend on the site of thrombosis. Tests of function
Bleeding time
Bleeding time was first developed as a test of platelet function by Duke in 1910. Dukes test measured the time taken for bleeding to stop from a standardized wound in the ear lobe which was blotted every 30 seconds. The normal time for bleeding to stop was less than 3 minutes. More modern techniques are now used. A normal bleeding time reflects sufficient platelet numbers and function, plus normal microvasculature. Multiple electrode aggregometry
In multiple electrode aggregometry, anticoagulated whole blood is mixed with saline and a platelet agonist in a single-use cuvette with two pairs of electrodes. The increase in impedance between the electrodes as platelets aggregate onto them, is measured and visualized as a curve.