Antiplatelet, Anticoagulant, Thrombolytic Agents

Antiplatelet, Anticoagulant, Thrombolytic Agents

Introduction

The video introduces the topic of blood thinning medications and encourages viewers to check out the website for additional resources.

Importance of Additional Resources

The video emphasizes the importance of following along with notes and illustrations provided on their website to enhance learning.

Phases of Hemostasis

The three primary phases of hemostasis are platelet plug formation, coagulation cascade, and fibrinolytic mechanisms. Anti-platelets, anticoagulants, and thrombolytics work in these three particular phases.

Platelet Plug Formation

  • Endothelial cells release nitric oxide and prostacycline to inhibit platelets.
  • When endothelial cells become damaged, they lose the ability to release nitric oxide and prostacycline.
  • Platelets bind to Von Willebrand factor in sub-endothelial layer when not inhibited by nitric oxide.
  • Anti-platelet agents can stop platelets from forming a plug.

Conclusion

The video concludes by emphasizing the importance of understanding how anti-platelets, anticoagulants, and thrombolytics work in different phases of hemostasis.

Platelet Activation and Granule Release

This section discusses the activation of platelets and the release of granules.

Von Wildebron Factor and GP1B Protein

  • Platelets are bound to collagen lining via Von Wildebron Factor.
  • Von Wildebron Factor is made by platelets and injured endothelial cells.
  • GP1B protein interacts with Von Wildebron Factor to bind with platelets.

Platelet Activation

  • Platelets become activated when there is no nitric oxide or prostacyclin by damaged endothelial cells.
  • Once activated, platelets start to release cytokines from their granules as an alarm system.
  • ADP (adenosine diphosphate), a molecule released by activated platelets, binds onto P2Y12 receptors on nearby platelets, increasing intracellular calcium levels.

Granule Release

  • Activated platelets secrete different molecules from their granules, including Vaughn Waldron factor, fibrinogen, and calcium.
  • The increase in intracellular calcium activates the expression of gp2b3a receptors on the surface of the playlist.
  • The gp2b3a receptors allow playlists to connect with each other forming a plug at the site of vessel injury.

Mechanisms of Platelet Activation

This section discusses the mechanisms of platelet activation.

Calcium and Granules

  • Increasing calcium activates granules to release Von Wildebrand factor, fibrinogen, and ADP.
  • Phospholipase A2 is activated by calcium and breaks down phospholipids into arachidonic acid which is then broken down into thromboxane A2.
  • Thromboxane A2 acts similarly to ADP in increasing intracellular calcium, activating gp2b3a proteins, and releasing molecules important for platelet activation.

Cyclic AMP

  • Cyclic AMP inhibits the increase in calcium levels.
  • An enzyme that regulates cyclic AMP may be able to increase calcium levels.

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