part 1.2 hemostasis

What is hemostasis

The natural process that stops bleeding after blood vessel injury, maintaining vascular integrity and balance between clotting and blood flow.

What are the steps in hemostasis

1. Vasoconstriction 2. Primary hemostasis (platelet plug formation) 3. Secondary hemostasis (coagulation) 4. Clot retraction and repair 5. Fibrinolysis.

What is vasoconstriction

A temporary narrowing of injured blood vessels that reduces blood flow and limits blood loss.

What are the key mechanisms of vasoconstriction

Endothelin release, extracellular matrix (ECM) exposure, and neurogenic/inflammatory mechanisms.

What is the role of endothelin in vasoconstriction

Damaged endothelium secretes endothelin which binds to smooth muscle receptors and induces vasoconstriction.

How does ECM exposure cause vasoconstriction

Exposure of the extracellular matrix triggers smooth muscle contraction as a protective reflex.

What is the neurogenic or inflammatory mechanism of vasoconstriction

Injury releases chemical mediators that activate pain receptors, triggering reflex smooth muscle contraction and vasoconstriction.

What happens in primary hemostasis

Platelets adhere, activate, and aggregate at a site of vessel injury to form a temporary seal.

Describe platelet adhesion

von Willebrand factor (vWF) binds to exposed collagen, and platelets attach via GP1b receptors.

Describe platelet activation

Platelets release ADP, thromboxane A2, and serotonin, which recruit more platelets and promote vasoconstriction.

Describe platelet aggregation

Activated platelets expose GP2b3a receptors that link together via fibrinogen or vWF bridges, forming a growing platelet mass.

What is secondary hemostasis

It is the coagulation cascade, a series of reactions where inactive clotting factors (zymogens) are sequentially activated after vessel injury.

Which clotting factors are Vitamin K–dependent

Factors II, VII, IX, and X.

Where are Vitamin K–dependent factors synthesized

In the liver, after Vitamin K from the intestine activates precursors by γ-carboxylation.

What is the effect of Vitamin K activation

It allows clotting factors to bind calcium (Ca²⁺), which is essential for coagulation.

Where are the active clotting factors released

Into the blood to participate in clot formation.

What inhibits the coagulation cascade

Antithrombin (ATIII), Protein C with Protein S, Tissue Factor Pathway Inhibitor (TFPI), and Protein Z.

What is the function of Antithrombin (ATIII)

It neutralizes thrombin (IIa) and Factors IXa and Xa.

What is the role of Protein C and Protein S

They are Vitamin K–dependent anticoagulants that deactivate Factors Va and VIIIa and enhance fibrinolysis by blocking plasminogen activator inhibitor (PAI).

How is Protein C activated

When thrombin binds to thrombomodulin on endothelial cells.

What does Tissue Factor Pathway Inhibitor (TFPI) do

It suppresses the TF–VIIa complex and directly inhibits Factor Xa.

What is the function of Protein Z with ZPI

It acts as a Vitamin K–dependent regulator that helps inactivate Factor Xa.

What is clot retraction and repair

It is the process where the wound edges are drawn closer together by platelet contraction involving actin and myosin.

What growth factors are released during clot repair

Platelet-Derived Growth Factor (PDGF) and Vascular Endothelial Growth Factor (VEGF).

What is the function of PDGF

It stimulates the renewal of damaged smooth muscle and connective tissue.

What is the function of VEGF

It helps regenerate the endothelial lining and promotes angiogenesis.

What is fibrinolysis

The breakdown of a fibrin clot once healing begins to restore normal blood flow.

What converts plasminogen to plasmin

Tissue plasminogen activator (tPA) bound to fibrin.

What does plasmin do

It degrades fibrin mesh, fibrinogen, Factors Va and VIIIa, vWF, HMWK, and other prothrombotic proteins.

What inactivates plasmin

α-antiplasmin, after which it is cleared from circulation by the liver.

What are fibrin degradation products (FDPs)

They are fragments generated when plasmin breaks down fibrin, indicating clot breakdown.