Summary

This document provides an overview of platelets and blood coagulation. It details the role of platelets in hemostasis, the mechanisms of platelet reactions, and the steps involved in blood clotting, including the intrinsic and extrinsic pathways.

Full Transcript

# Physiology - Platelets ## Platelets Platelets, or thrombocytes, are small, colorless cell fragments in our blood that form clots and stop or prevent bleeding. Platelets are made in our bone marrow. Life span is 8 days. ## 1. Constriction of blood vessels * Constriction of blood vessels occurs...

# Physiology - Platelets ## Platelets Platelets, or thrombocytes, are small, colorless cell fragments in our blood that form clots and stop or prevent bleeding. Platelets are made in our bone marrow. Life span is 8 days. ## 1. Constriction of blood vessels * Constriction of blood vessels occurs immediately after injury of vessels to decrease blood loss from the injured site. * **Causes of vasoconstriction:** * **Local myogenic contraction** due to direct trauma. * **Nervous reflexes** start due to pain from the injured vessel. * **Local humoral factors** liberated from platelets such as: * ADP * Serotonin * Thromboxane A2 ## 2. Formation of a temporary hemostatic plug * **Hemostatic plug** is an aggregation of platelets formed during early stages of hemostasis. * Injury of the vessel stimulates the platelets to form the mechanical plug to seal the vascular injury. ## Platelet reactions in hemostasis 1. **Platelet adhesion:** After blood vessel injury platelets adhere to the exposed subendothelial collagen. 2. **Platelet activation:** After adhesion, platelets swell, change their shape, and discharge the contents of granules. 3. **Platelet release reaction:** Platelet release content of its granules which have a role in clot formation. * ADP * Serotonin * Thromboxane A2 4. **Platelet aggregation:** Platelet aggregation, the process by which platelets adhere to each other at sites of vascular injury, has long been recognized as critical for hemostatic plug formation and thrombosis. 5. **Platelet fusion:** Irreversible slow process, in which the aggregated platelets fuse at the site of injury. * Platelet fusion is caused by: * High concentration of ADP * Thrombin ## Blood coagulation * The clotting mechanism is the process of conversion of temporary platelets plug into definitive clots by fibrin. * **Coagulation factors** are plasma proteins that are synthesized by the liver. * The **coagulation cascade** involves several steps of activation of clotting factors. * The final step of coagulation is the formation of **fibrin mesh**. ## Blood coagulation - Diagram The diagram illustrates how blood clots formed by the intrinsic and extrinsic pathways. * **Intrinsic Pathway:** This pathway is triggered by a change in the blood itself, such as the presence of collagen. * **Extrinsic Pathway:** This pathway is triggered by an external factor, such as trauma to the blood vessel. ### Intrinsic Pathway 1. HMWK and PK activate Factor XII 2. Factor XIIa activates Factor XI 3. Factor XIa activates Factor IX 4. Factor IXa, along with Factor VIIIa activate Factor X 5. Factor Xa, along with Factor Va, convert prothrombin (Factor II) into thrombin (Factor IIa) 6. Thrombin (Factor IIa) converts fibrinogen into fibrin, which forms the clot. 7. Factor XIIla cross-links fibrin, strengthening the clot. ### Extrinsic Pathway 1. Trauma leads to the release of tissue factor (TF) from damaged cells 2. TF activates Factor VII 3. Factor VIIa, along with Factor Xa, activates Factor X 4. Factor Xa, along with Factor Va, convert prothrombin (Factor II) into thrombin (Factor IIa) 5. Thrombin (Factor IIa) converts fibrinogen into fibrin, which forms the clot. 6. Factor XIIla cross-links fibrin, strengthening the clot. The diagram shows the various factors and enzymes involved in both pathways, along with the final formation of the fibrin mesh. # Thanks

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