18.5 Hemostasis

Hemostasis is the body's way of stopping bleeding. It's like your blood's emergency response team, springing into action when a blood vessel is damaged. This process involves three main steps: vascular spasm, platelet plug formation, and blood clotting.

Understanding hemostasis is crucial for grasping how the body maintains its internal environment. It's a delicate balance – too little clotting leads to excessive bleeding, while too much can cause dangerous blood clots. This topic connects the circulatory system to our body's defense mechanisms.

Hemostasis

Mechanisms of hemostasis

Top images from around the web for Mechanisms of hemostasis

• 

  Hemostasis | Boundless Anatomy and Physiology View original

  Is this image relevant?

• 

  Hemostasis · Anatomy and Physiology View original

  Is this image relevant?

• 

  Coagulation - Wikipedia View original

  Is this image relevant?

• 

  Hemostasis | Boundless Anatomy and Physiology View original

  Is this image relevant?

• 

  Hemostasis · Anatomy and Physiology View original

  Is this image relevant?

1 of 3

Top images from around the web for Mechanisms of hemostasis

• 

  Hemostasis | Boundless Anatomy and Physiology View original

  Is this image relevant?

• 

  Hemostasis · Anatomy and Physiology View original

  Is this image relevant?

• 

  Coagulation - Wikipedia View original

  Is this image relevant?

• 

  Hemostasis | Boundless Anatomy and Physiology View original

  Is this image relevant?

• 

  Hemostasis · Anatomy and Physiology View original

  Is this image relevant?

1 of 3

• Vascular spasm occurs immediately after injury causing vasoconstriction of damaged blood vessels which reduces blood flow to the injured area and helps limit blood loss
• Platelet plug formation involves platelets adhering to exposed collagen in the damaged vessel wall, releasing chemicals that attract more platelets, and aggregating to form a plug that seals the damaged vessel (primary hemostasis)
• Coagulation (blood clotting) is activated by the coagulation cascade, leading to the formation of fibrin strands that strengthen the platelet plug and create a stable clot to prevent further blood loss (secondary hemostasis)
  • This process involves various clotting factors, which are proteins that work together to form the clot

Extrinsic vs intrinsic coagulation pathways

• Extrinsic pathway is triggered by tissue factor (factor III) released from damaged tissues, involves factor VII, acts faster than the intrinsic pathway, and is the primary pathway for initiating coagulation
• Intrinsic pathway is triggered by contact with negatively charged surfaces (collagen, glass), involves factors XII, XI, IX, and VIII, acts slower than the extrinsic pathway, and amplifies the coagulation process
• Both pathways converge at the common pathway (factor X activation), lead to the activation of prothrombin (factor II) to thrombin, which converts fibrinogen (factor I) to fibrin that forms a stable clot

Regulation of hemostasis

• Fibrinolysis is the process of breaking down blood clots to prevent excessive clotting and maintain normal blood flow
• Anticoagulants are substances that prevent or reduce blood clotting
  • Heparin is a naturally occurring anticoagulant that enhances the activity of antithrombin III, inhibiting several clotting factors
  • Warfarin is a synthetic anticoagulant that interferes with vitamin K-dependent clotting factor synthesis

Disorders of hemostasis

• Hemophilia is a genetic disorder causing deficiency in factor VIII (hemophilia A) or factor IX (hemophilia B), impairing the intrinsic pathway, leading to prolonged clotting times, excessive bleeding, and difficulty forming stable clots
• von Willebrand disease is caused by a deficiency or dysfunction of von Willebrand factor (vWF), which is essential for platelet adhesion to the damaged vessel wall, causing impaired platelet plug formation and prolonged bleeding
• Thrombocytopenia is a low platelet count in the blood caused by decreased platelet production, increased destruction, or sequestration, leading to impaired platelet plug formation and increased risk of bleeding
• Disseminated intravascular coagulation (DIC) is a systemic activation of the coagulation cascade triggered by severe infections, trauma, or certain cancers, resulting in widespread clotting, consumption of clotting factors, and both thrombosis and bleeding due to depletion of clotting factors and platelets