2. Without looking into the text listen to the recording.

Say what information you have gathered.

Listen to the text again.

Now, read the text silently, trying to grasp alt the details of the contents.

Then, read it simultaneously with the speaker, trying to catch up with the tempo.

After that read the text aloud, trying to imitate the intonation.

Thrombosis is a typical pathological process of supravital forming a conglomerate (thrombus) consisting of plasma proteins and blood cells primarily attached to the injured inner surface of the blood vessel or heart cavities.

A thrombus should be distinguished from a blood clot: a clot may be generated in vivo and in vitro, whereas a thrombus may be generated only within a cardio-vascular system; from the very beginning of its formation a true thrombus is continuously fastened to the inner surface of the wall of a blood vessel or heart cavity, whereas a clot may be formed inside the vessel, unattached to the wall.

There are three conditions determining the formation of a thrombus ("The Virchow triad"): damage of the vessel wall, slowing down of the velocity of the blood stream, and changes in blood composition.

The stages of thrombosis are: agglutination, coagulation, retraction.

Thrombosis is one of the components of tissue response to injury. It is a local reversible process necessary for an adequate hemostasis, which prevents hemorrhage and blood loss and restores the wall of the blood vessel. Thrombosis in itself is a component of several other, more complex, pathologic processes such as inflammation, allergy, etc.

After a blood vessel injury, the von Willebrand factor (vWF) from the injured endotheliocytes functions as an adhesion bridge between subendothelial collagen and the Ib glycoprotein (Gplb) platelet receptor (primary reversible aggregation). The aggregation is accomplished through the fibrinogen binding to platelet Gp IIb-IIIa receptors and bringing many platelets together (secondary irreversible aggregation).

Congenital deficiencies in various receptors, or in bridging molecules, called factors (f), lead either to Glanzmann² thrombasthenia (deficiency of Gp IIb-IIIа receptors), or to Bernard-Soulier syndrome (deficiency of Gp Ib receptor), or to von Willebrand disease (deficiency of vWF). The initial reaction complex consists of an enzyme (f. IXa), a substrate (f. X) and a reaction accelerator (f. VIIIa) which are assembled on the phoshpolipid surface of platelets. Calcium ions (f. IV) hold the assembled components together and are essential for the reaction. The activated f. Xa then becomes the enzyme part of the second adjacent complex in the coagulation cascade, converting the prothrombin (f. II, substrate) to thrombin (f. IIa) in cooperation with, the reaction accelerator (f. Va). Thrombin converts fibrinogen to fibrin within and around the platelet plug, essentially cementing the platelets in place.

¹ Erik Adolf von Willebrand, Finnish internist, born February 1, 1870, Vaasa; Russia, died December 12, 1949, Perna, Finland.

²Eduard Glanzmann, Swiss paediatrician, born April 12, 1887, Luzern; died February 2, 1959.