Haemostasis Coagulation Dvt Pe Notes

Semester 2

Case 8: The Grocer

• What is the structure & function of platelets?

[1] Platelets (AKA: Thrombocytes) are minute discs that are formed in the bone marrow from megakaryocytes – extremely large calls of the haematopoietic series in the marrow. Platelets have many functional characteristics of whole cells, even though they do not have nuclei & cannot reproduce. In their cytoplasm are such active factors as:

• Actin & myosin molecules, which are contractile proteins similar to those found in muscle cells, and another contractile protein, thrombosthenin, that can cause the platelets to contract

• Residuals of both the endoplasmic reticulum & the Golgi apparatus that synthesise various enzymes and especially store large quantities of calcium ions

• Mitochondria & enzyme systems that are capable of forming ATP & ADP

• Enzyme systems that synthesise prostaglandins, which are local hormones that cause many vascular & other local tissue reactions

• A protein called fibrin-stabilising factor

• A growth factor that causes vascular endothelial cells, vascular smooth muscle cells, and fibroblasts to multiply & grow, thus causing cellular growth that eventually helps repair damaged vascular walls.

The cell membrane of the platelets is also important. On its surface is a coat of glycoproteins that repulses adherence to normal endothelium and yet causes adherence to injured areas of the vessel wall, especially to injured endothelial cells and even more so to any exposed collagen from deep within the vessel wall. The membrane also contains large amounts of phospholipids that activate multiple stages in the blood-clotting process.

Thus, the platelet is an active structure. It has a half-life in the blood of 8-12 days, so that over several weeks its functional processes run out. Then it is eliminated from the circulation mainly by the tissue macrophage system. >50% of the platelets are removed by macrophages in the spleen, where the blood passes through a latticework of tight trabeculae.

Under an electron microscope, activated platelets appear green, and inactive platelets appear blue.

• How does haemostasis & blood coagulation work?

Haemostasis = Prevention of blood loss.

Whenever a vessel is severed or ruptured, haemostasis is achieved by several mechanisms:

Vascular constriction Formation of a platelet plug Formation of a blood clot as a result of blood coagulation Eventual growth of fibrous tissue into the blood clot to close the hole in the vessel permanently

Vascular Constriction

Formation of the Platelet Plug

If the cut in a blood vessel is very small, then it is often sealed by a platelet plug, rather than by a blood clot. When platelets come in contact with a damaged vascular surface, especially with collagen fibres in the vascular wall, the platelets themselves immediately change their own characteristics drastically:

• They begin to swell

• They assume irregular forms with numerous irradiating pseudopods (temporary projections of the cytoplasm) protruding from their surfaces

• Their contractile proteins contract forcefully and cause the release of granules that contain multiple active factors

• They become sticky so that they adhere to collagen in the tissues via GP1b & to a protein called von Wille-brand factor that leaks into the traumatised tissue from the plasma

• They secrete large quantities of ADP, which attracts more platelets &stimulates their degranulation (positive feedback)

• Their enzymes form thromboxane A, which promotes platelet aggregation, degranulation, & vasoconstriction (positive feedback)

The ADP and thromboxane in turn act on nearby platelets to activate them as well, and the stickiness of these additional platelets causes them to adhere to the original activated platelets. Therefore, at the site of any opening in a blood vessel wall, the damaged vascular wall activates successively increasing numbers of platelets that themselves attract more and more additional platelets, thus forming a platelet plug. At first this is a loose plug, but it is usually successful in blocking blood loss if the vascular opening is small. Then, during the subsequent process of blood coagulation, fibrin threads form. These attach tightly to the platelets, thus constructing an unyielding plug.

Blood Coagulation in the Ruptured Vessel

Severe trauma to vascular wall Clot begins to develop within 15-20seconds.

Minor trauma to vascular wall Clot begins to develop within 1-2minutes.

Activator substances (clotting factors) from the traumatised vascular wall, from platelets, and from blood proteins adhering to the traumatised vascular wall initiate the clotting process.

Within 3-6minutes after vessel rupture, if the opening isn’t too large, the entire opening or broken end of the vessel is filled with clot.

After 20-60minutes, the clot retracts; this closes the vessel still further.

Growth of Fibrous Tissue into the Blood Clot

Once a blood clot has formed, it can follow one of two courses:

• It can become invaded by fibroblasts, which subsequently form connective tissue all through the clot – Usual in a clot that forms due to a small hole. Begins within a few hours after the clot is formed, which is promoted at least partially by growth factor secreted by platelets. This continues to complete organisation of the clot into fibrous tissue within about 1-2weeks.

• Or, it can dissolve – When excess blood has leaked into the tissues and tissue clots have occurred where they aren’t needed, special substances within the clot itself usually become activated. These function as enzymes to dissolve the clot.

Mechanism of Blood Coagulation

Procoagulants promote coagulation. Anticoagulants inhibit coagulation.

Whether blood will coagulate depends on the balance between these 2 groups of substances.

In the bloodstream, the anticoagulants normally predominate, so that the blood doesn’t coagulate whilst it is circulating in the blood vessels. When a vessel is ruptured,...

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