Lecture 6

Flashcards on the key vocabulary and concepts from the lecture on secondary hemostasis and blood clot formation.

Blood Clotting

The process by which blood is transformed into a solid gel.

Blood Clot/Thrombus

A solid gel formed from blood, also known as a thrombus, consisting of the protein fibrin.

Fibrin

A protein that is the essential part of a blood clot.

Secondary Hemostasis

Occurs after platelet plug formation and involves a cascade of enzyme activation leading to a fibrin clot.

Clotting Factors

Inactive plasma proteins in the blood that are essential for blood clotting.

Calcium

Ionized calcium (Factor IV), which is essential for many activation reactions in blood clotting.

Activion of Thrombin Enzyme

The key step in clot formation pathway; inactive prothrombin is converted to thrombin by the prothrombinase complex.

Thrombin

Active enzyme that converts fibrinogen to fibrin.

Fibrin

An insoluble protein that forms a mesh-work, trapping cells to form a clot.

Intrinsic Pathway

Involves factors from within the blood and blood vessel itself.

Extrinsic Pathway

Initiated by factors outside the blood vessel.

Common Pathway

The point where the intrinsic and extrinsic pathways converge to activate factor X, leading to clot formation.

Contact Activation Factor

Factor XII, activated by contact with a damaged blood vessel wall, initiating the intrinsic pathway.

Extrinsic Pathway Activation

Activated when factor VII comes into contact with tissue products and tissue factors outside a blood vessel.

Tissue Factors

Located on the outer plasma membrane of various tissue cells and activate factor VII when exposed to blood after vessel damage.

TFPI (Tissue Factor Pathway Inhibitor)

Inhibits tissue factor (factor III), which initiates the extrinsic pathway.

Antithrombin 3

Inhibits the actions of thrombin.

Thrombomodulin

A protein on healthy endothelial cells that binds to thrombin, activating protein C which then inhibits factors Va and VIIIa.

Calcium Chelators

Bind ionized calcium, preventing activation of clotting factors.

Heparin

Increases the activity of antithrombin 3.

Vitamin K Antagonists

Inhibit the synthesis of vitamin K-dependent clotting factors (II, VII, IX, X).

Fibrinolysis

The enzymatic breakdown of fibrin in blood clots.

Plasminogen Activators (e.g., tPA)

Convert plasminogen to plasmin, which breaks down fibrin.

Plasmin

Breaks down insoluble fibrin strands into soluble fibrin degradation products to dissolve the clot.

Thrombolytics

Drugs used to dissolve major clots quickly, restoring blood flow (e.g., in heart attacks).

Thrombocytopenia

A deficiency in the number of platelets.

von Willebrand’s Factor

A plasma protein secreted by endothelial cells and platelets that promotes adhesion by binding to platelets and exposed collagen.

Thrombosis

Formation of a blood clot in a vessel, blocking blood flow.

When pro-hemostatic factors fail

Severe bleeding disorders, leading to hemorrhage

Defects in pro-hemostatic pathways include: Thrombocytopenia (deficiency in the number of platelets), deficiency of von Willebrand’s factor (a plasma protein secreted by endothelial cells and platelets that promotes adhesion), Problems with clotting factors: Hereditary deficiencies of clotting factors, A lack of vitamin K may cause deficiencies of factors requiring vitamin K for their synthesis.

Tissue Plasminogen Activator (tPA)

Released from healthy endothelial cells; used as clinical clot busters (thrombolytics) to dissolve clots in heart attack patients.

Calcium chelators (e.g., sodium citrate)

Bind ionized calcium, preventing the activation of clotting factors.

Heparin

Increases the activity of antithrombin III.

Vitamin

Inhibit the synthesis of vitamin K-dependent clotting factors (factors II, VII, IX, and X).