Lecture 5

Flashcards covering platelets and hemostasis, including key factors, steps, and related concepts.

Hemostasis

The prevention of blood loss.

Platelets

Cell fragments found in the buffy coat of blood, important for hemostasis.

Pro-hemostatic factors

Factors that prevent blood loss.

Anti-hemostatic factors

Factors that keep the blood fluid.

Vasoconstriction

The contraction of a ruptured blood vessel to minimize blood loss; the first step of hemostasis.

Primary hemostasis

The second step of hemostasis, where platelets aggregate to form a platelet plug (white thrombus).

Secondary hemostasis

The third step of hemostasis, also known as blood clotting or coagulation (red thrombus), where blood clotting enzymes are activated to form a stronger gel-like clot.

Thrombus

A blood clot.

Platelets/Thrombocytes Origin

Originate from pluripotent stem cells of the bone marrow, which are converted to megakaryocytes. Platelets are pinched off from the cytoplasm of megakaryocytes.

Alpha granules

Vesicles in platelets containing large molecules like von Willebrand factor, growth factors, some blood clotting factors, and cytokines.

Dense granules

Vesicles in platelets containing small molecules like ADP, ATP, serotonin, and calcium.

von Willebrand factor

An adhesive protein secreted by platelets and endothelial cells that facilitates platelet adhesion to collagen tissue at the site of a blood vessel injury.

Platelet Activation

Binding of platelets to collagen triggers the release of chemicals (ADP and serotonin) which act locally to change platelet metabolism, shape, and receptor expression.

Fibrinogen receptor

Expressed on the surface of activated platelets. Binds to fibrinogen, a plasma protein, to form a network that ultimately forms the platelet plug.

Thromboxane A2 & ADP

Secreted by activated platelets to attract more platelets to the cut site and continue aggregation.

Serotonin (5HT)

Acts as a vasoconstrictor when secreted from activated platelets.

Thromboxane A2

Promotes further platelet aggregation and vasoconstriction of the vascular smooth muscle.

Prostacyclin and Nitric Oxide

Inhibit the spread of the platelet plug along undamaged endothelium.

Arachidonic acid

Produced from membrane phospholipids due to membrane damage, initiating the formation of the platelet plug.

Lipoxygenase pathway

Converts arachidonic acid to leukotrienes, initiating inflammatory responses.

Cyclooxygenase pathway

Converts arachidonic acid to prostaglandins, playing a role in hemostatic effects.

COX 1

Cyclooxygenase enzyme isoform found in platelets that produces thromboxane A2.

COX 2

Cyclooxygenase enzyme isoform found in healthy endothelial cells that results in the synthesis of prostacyclin.

Aspirin

Inhibits both COX-1 and COX-2, blocking thromboxane A2 production in platelets and prostacyclin production in endothelial cells, affecting hemostasis.