Pathology > Basic Hematology > Normal Hematopoiesis > Platelet Function

Platelet: Function

Platelets play a key role in maintaining vascular integrity by sealing vessels with damaged endothelium and initiating the repair process.

Platelet: Function

Starting at LEFT, CLICK on the above images to review normal platelet function.

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Normal platelets in the blood stream have a discoid shape and have little or no interaction with other platelets or endothelium.

Endothelial damage, specifically exposure of underlying collagen as shown at left, triggers platelet adhesion. First, von Willebrand's factor(vWF) binds to subendothelial collagen. This results in conformational changes in vWF allowing vWF to bind to the GP Ib receptor on platelets.

Exposure of the basement membrane and release of tissue factor from damaged endothelialcells serves to activate coagulation pathways.

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Following adhesion, proteins and soluble products interact with platelet membrane receptors to cause activation. At time of activation, platelets become spherical and develop cytoplasmic hair-like filipodia. The GP IIb/IIIa receptor complex Ds conformation allowing binding of fibrinogen. The contents of the alpha and dense granules are secreted. All of the above lead to platelet aggregation.

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At left you see vWF bound to collagen; vWF bound to platelet GP Ib, and fibrinogen bound to activated platelet GP IIb/IIIa. The fibrinogen acts as a glue binding platelets together.

The contents of platelet granules are discharged, exponentially magnifying the accumulation of platelets and fibrin at the site of injury. This process is known as platelet aggregation, the end result of which is formation of a platelet-fibrin plug or thrombus.

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The fibrin gives the platelet mass strength allowing it to function as a secure patch and a protected base for repair and healing.

Note that many of the platelets appear as empty sacks having discharged their granules.

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Clot retraction is a function in which the central portion of the platelet attaches to fibrin strands at nodes (cross-over points)and platelet filipods attach to single fibrin strands. Actin in the filipods and myosin in the platelet body contract, shortening the fibrin strands and shinking the platelet-fibrin plug.This process requires large amounts of energy (platelet ATP) and calcium.

Add Ca++ by pushing the button below and observe the contraction.

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