Glossary: Basics of Haemostasis Online Training

Glossary Text

α1-Antitrypsin Protein serving as a protease inhibitor.

α2-Antiplasmin α2-Antiplasmin is a serine protease inhibitor targeting Plasmin and

forming a Plasmin - Antiplasmin complex leading to the irrevesible

inhibition of Plasmin.

α2-Makroglobulin Inhibitor of the fibrinolysis and Thrombin. Appears also as acute

phase protein.

AA Arachidonic acid is an unsaturated fatty acid, which is synthesised

from phospholipids of the cells by the phospholipase A2. Arachidonic

acid synthesised from the platelets is catalysed by cyclooxygenase

(COX) to thromboxane A2 (TXA2), which then promotes platelet

activation, while when synthesised from endothelial cells it becomes

prostaglandin I2 (PGI2), which inhibits platelet activation.

Adhesion receptor Group of receptors in the plasma membrane of cells, showing the

adhesion of cells to extracellular matrix and blood plasma proteins,

adhesion between heterogeneous cells, or indirect ligand-mediated

adhesion between like cells (homotyped adhesion).

ADP Adenosine Di-Phosphate plays an important role in thrombus

formation. ADP is stored in the granules of the platelets and is

secreted into the plasma upon their activation. This leads to a

positive amplifier loop, which activates further platelets. Additional

ADP is released from the ATP of platelets, erythrocytes and other

cells in the area of tissue damage. This and the local suppression of

the ADP inhibitors at the site of tissue damage provides a local

accumulation of ADP and thus promotes aggregation.

Glossary Text

Amplification Amplification is the second phase in the coagulation process and

starts with platelets being activated by small amounts of Thrombin.

Anti-fibrinolytic-system Group of proteins regulating fibrinolysis.

Anti-thrombotic-system Group of proteins regulating clot formation.

Antihemophilic globulin Factor VIII and/or Factor IX.

Antithrombin Antithrombin is an important inhibitor in plasmatic coagulation,

inhibiting Thrombin (Factor IIa) and Factor Xa mainly, but also all

other coagulation factors as well as Plasmin, TF-Factor VIIa complex

and Kallikrein. The inhibitory potential of Antithrombin is increased

dramatically by heparan sulfate. Antithrombin is synthesised in the

liver and under physiological conditions is found in blood at

concentrations of 70 - 120 %.

APC resistance APC resistance is the inability of activated Protein C to cleave Factor

Va causing a persisting ability of Factor Va in activating Prothrombin

to Thrombin. Individuals with Factor V Leiden show an significant

increased risk of thrombotic events.

Apixaban Drug which belongs to a group of Direct Oral Anti Coagulants that

inhibiting the coagulation Factor Xa directly.

ASA Acetylsalicylic acid is a widely used analgesic, anti-inflammatory,

antipyretic and antiplatelet drug. It inhibits the cyclooxygenase

irreversibly.

Ca++ = Ca2+ Ca++ (= Factor IV) has an essential function in the activation of

Factor II, VII, IX and X. The calcium ions bridge the gap between the

negatively charged clotting factor and the negatively charged

phospholipids of the platelets or cells, which cannot bind to each

other without the mediation by calcium due to their equal charge.

Calcium also plays an important role in adhesion and aggregation of

the platelets, as well as muscle contraction.

Glossary Text

Calcium Calcium is a chemical element in the periodic table of elements with

the symbol Ca and the atomic number 20. As an essential part of

living matter Calcium is involved in the construction inter alia bones

and teeth. In addition to K +, Na +, Ca++ plays an important role in

the transmission of stimuli in nerve cells and in signal transduction in

other cells. Ca++ in haemostasis has an important mediator role.

Calcium-cation Calcium is a chemical element in the periodic table of elements with

the symbol Ca and atomic number 20. As an essential part of living

matter Calcium is involved in constructing inter alia bones and teeth.

Alongside K+ and Na+, Ca++ plays an important role in transmitting

stimuli in nerve cells and in signal transduction in other cells. In

haemostasis Ca++ has an important mediator role.

Calcium-ion Calcium is a chemical element in the periodic table of elements with

the symbol Ca and atomic number 20. As an essential part of living

matter Calcium is involved in constructing inter alia bones and teeth.

Alongside K+ and Na+, Ca++ plays an important role in transmitting

stimuli in nerve cells and in signal transduction in other cells. In

haemostasis Ca++ has an important mediator role.

Carboxy group The carboxy group in chemistry is the functional group of the

carboxylic acids, consisting of one carbon, two oxygen and one

hydrogen atom.

Carboxylation Carboxylation is a chemical reaction in which a carboxylic acid group

is produced by treating a substrate with carbon dioxide.

Catalytic center The active site is the area of the catalytic effect of an enzyme.

Christmas-factor Factor IX, a vitamin-K depending pro-enzyme of the serine protease

Factor IXa, activating Factor X to Factor Xa in the tenase complex.

Synthesised in the liver, under normal physiological conditions in

blood it is found at concentrations of 70 - 120 %.

Clopidogrel Drug inhibiting the ADP receptor P2Y12 and subsequently ADP-

induced platelet aggregation.

Cofactor In haemostasis a coagulation factor without enzymatic function.

Glossary Text

Collagen Collagen is a protein that is mainly part of the connective tissue. It is

the most important fibre component of the skin, cartilage, bones,

tendons, teeth and blood vessels. Collagen of the blood vessels is

not exposed to blood under physiological conditions. In case of injury

to the endothelial layer of the blood vessels, the collagen is exposed

to the platelets and triggers their adhesion and aggregation.

Collagen is therefore the central activator of primary haemostasis.

COOH Carboxy group is the functional group of carboxylic acids, consisting

of one carbon, two oxygen and one hydrogen atom.

COX1 Cyclooxygenase-1 (COX1) is an enzyme that converts arachidonic

acid into thromboxane A2 and prostaglandin I2. It occurs in all tissue

types. Acetylsalicylic acid inhibits the activity of cyclooxygenase

irreversibly.

Cyclooxygenase COX for short. Enzyme catalysing the prostaglandins. Appears in

two iso-forms. COX1 induces the synthesis of Thromboxane in

platelets. COX2 induces the synthesis of prostaglandins in white

blood and endothelia cells.

D-Dimer Product of the fibrin cleavage by Plasmin. Elevated D-Dimer levels

indicating increased pro-coagulation activities in the human body.

Dabigatran Drug which belongs to a group of Direct Oral AntiCoagulants which

inhibits the coagulation Factor IIa (Thrombin) directly.

DOAC Is a group of drugs inhibiting a coagulation factor directly without a

cofactor. Most common DOACs are inhibitors to Factor IIa

(Thrombin, also called Direct Thrombin Inhibitors) and to Factor Xa

(also called Direct Factor Xa Inhibitors (DXaI)).

Extrinsic tenase

complex

Complex of coagulation factors activating the coagulation Factor X.

Factor II Prothrombin. Vitamin-K dependent pro-enzyme of the serine

protease Factor IIa (Thrombin) converting Fibrinogen to Fibrin.

Synthesised in the liver, under physiological conditions it is present

in the blood at concentration of 70 - 120 %.

Glossary Text

Factor IIa Factor IIa (= Thrombin) is a central component of plasmatic

coagulation and reaction partner of a variety of substrates. Under

physiological conditions, Thrombin is not found in free form in the

bloodstream. The inactive form of Thrombin is Prothrombin (Factor

II) which is synthesised in the liver. Thrombin activates a number of

coagulation factors, is a potent platelet activator, and activates the

antithrombotic system. Thrombin acts on the fibrinogen and cleaves

the fibrinopeptides A and B from the fibrinogen molecule, causing

polymerisation of fibrin and forming the fibrin net.

Factor V Also Proaccelerin. Factor V is the inactive form of coagulation Factor

Va and is activated by Thrombin (Factor IIa). Factor Va together with

Factor Xa forms the prothrombinase complex (with Ca++ and

phospholipids), with Factor Va acting as a cofactor. By complexing

with Factor Xa, the activation of Thrombin is accelerated a thousand

fold. Factor V is synthesised in the liver and is present in plasma at a

concentration of 60-150%. The most important inhibitor of Factor Va

is the Protein C / Protein S complex system. The inability of the

activated Protein C to cleave the Factor Va leads to an increased

risk of thrombosis (APC resistance, Factor V Leiden).

Factor Va Accelerine, cofactor of serine protease Factor Xa, activating together

with Factor Xa, CA++ and phospholipids in the prothrombinase

complex Prothrombin to Thrombin. Synthesised in liver,

megacaryocytes and endothelium cells, under physiological

conditions it is present in the blood in blood at concentrations of 60 -

150 %.

Factor VI Historically an independent coagulation factor. However, research

has shown Factor VI is identical to Factor V, so that Factor VI is not

used anymore.

Factor VII Vitamin-K depending pro-enzyme of the serine protease Factor VIIa

activating the coagulation Factors IX, X, VII, II (Prothrombin) and X

mostly in a complex with Tissue Factor. Synthesised in liver and

under physiological conditions it is present in blood at concentrations

of 60 - 170 %.

Glossary Text

Factor VIIa Vitamin-K depending serine protease activating the coagulation

Factors IX, X, VII, II (Prothrombin) and X mostly in a complex with

Tissue Factor. Synthesised in liver and under physiological

conditions it is present in blood at concentrations of 60 - 170 %.

Factor VIII Anti-haemophilic factor A, pro-enzyme of the cofactor VIIIa, together

with the serine protease Factor IXa, CA++ and phospholipids it

activates the coagulation Factor Xa. Synthesised in liver and carried

in the blood bound to von Willebrand Factor (vWF). Under

physiological conditions is present in blood at concentrations of 50 -

150 %.

Factor VIIIa Anti-haemophilic Factor A, cofactor to serine protease Factor IXa,

activating together in a complex with the serine protease Factor IXa,

CA++ and phospholipids the coagulation Factor Xa. Synthesised in

the liver and carried in the blood bound to von Willebrand Factor

(vWF). Under physiological conditions in blood at concentrations of

50 - 150 %.

Factor IX Factor IX (= Christmas factor or antihemophilic globulin B) is the

inactive form of coagulation Factor IXa. Factor IXa, together with its

Cofactor VIIIa, forms the tenase complex (with Ca++ and

phospholipids). Primarily, the complex of TF and Factor VIIa

activates Factor IX. Factor IX is synthesised in the liver and is

present in plasma at a concentration of 70-120%. The most

important Factor IXa inhibitor is Antithrombin. The most prominent

disorder of Factor IX is haemophilia B.

Factor IXa Christmas-Factor. Vitamin-K dependent serine protease, activating

Factor X to Factor Xa in the tenase complex.

Factor X Stuard-Prower Factor. Vitamin-K dependent pro-enzyme of the

serine protease Factor Xa which is activating Factor II (Prothrombin)

to Factor IIa (Thrombin) in the prothrombinase complex with

Cofactor Va, Ca++ and phospholipids.

Glossary Text

Factor Xa Stuard-Prower Factor. Vitamin-K depending serine protease

activating Factor II (Prothrombin) to Factor IIa (Thrombin) in the

prothrombinase complex with cofactor Va, Ca++ and phospholipids.

Factor XI Rosenthal Factor. Pro-enzyme of the serine protease Factor XIa

which activates Factor IX to Factor IXa. Factor XI is synthesised in

the liver and under physiological conditions it is present in blood at

concentrations of 70 - 120 %.

Factor XIa Rosenthal Factor. Serine protease activating Factor IX to Factor IXa

is synthesised in the liver, under physiological conditions it is present

in the blood at concentrations at 70 - 120 %.

Factor XII Hageman Factor. Pro-enzyme of the serine protease Factor XII

which activates Factor XI to Factor XIa and Factor VII to Factor VIIa.

Synthesised in the liver Factor XII under physiological conditions it is

present in blood at concentrations at 70 - 120 %, but might show

individual variances.

Factor XIIa Hageman factor. Serine protease activating Factor XI to Factor XIa

and Factor VII to Factor VIIa. Synthesised in the liver, Factor XIIa

under physiological conditions is present in the blood at

concentrations at 70 - 120 %, but might show individual variances.

Factor XIII Fibrin stabilising factor. Pro-enzyme of Factor XIIIa. Activated by

Thrombin (Factor IIa) induces Factor XIIIa the crosslinking of the

fibrin. Synthesised in Megacaryocytes, Macrophagues, placenta and

liver. Under physiological conditions it is present in blood at

concentrations at 70 - 140 %.

Factor XIIIa Fibrin stabilising factor. Activated by Thrombin (Factor IIa) induces

Factor XIIIa the crosslinking of the fibrin. Synthesised in

Megacaryocytes, Macrophagues, placenta and liver. Under

physiological conditions it is present in the blood at concentrations at

70 - 140 %.

Glossary Text

Factor-V-Leiden-

Mutation

Mutation of GI691A in Exon 10 of the Factor V gene resulting in the

replacement of Arginin by Glutamine in position 506. Subsequently,

activated Protein C doesn't find the cleavage area of the Factor Va

causing a persisting ability of Factor Va in activating Prothrombin to

Thrombin. Individuals with Factor V Leiden have a significant

increased risk of thrombotic events.

Fibrin Final product of the plasmatic coagulation resulting from the

cleavage of Fibrinopeptid A and B from the E-fragment of the

fibrinogen molecule induced by Thrombin. Fibrin acts as a biological

glue sealing the area of endothelial damage covered by platelets.

Fibrinogen Fibrinogen is the water-soluble precursor of fibrin, which forms the

matrix for wound closure. Fibrinogen is synthesised in the liver

(hepatocytes) and occurs predominantly in the blood. It is also stored

in the alpha granules of the platelets. Other storage locations are

cells of the cellular matrix and body fluids (e.g. lymph). The

reference range of fibrinogen is 1.6 to 4.0 g / L. At fibrinogen levels

<0.5 g / L, bleeding tendency increases with decreasing fibrinogen

concentrations. An increased concentration can be found during

inflammatory processes.

Fibrin stabilising factor Factor XIII/ Factor XIIIa. Activated by Thrombin (Factor IIa) induces

Factor XIIIa the crosslinking of the fibrin. Synthesised in

Megacaryocytes, Macrophagues, placenta and liver. Under

physiological conditions it is present in blood at concentrations at 70

- 140 %.

Fibrinogen receptor Integrin ɑ2bβ3 or GP IIb/IIIa. The glycoprotein IIb/IIIa complex is the

receptor for fibrinogen and von Willebrand Factor. Fibrinogen binding

to this receptor at the surface of the platelets allows a robust

agglutination of the platelets.

Fibrinolytic system Processes and agents involved to cleave the thrombus or fibrin clot.

The fibrinolytic system includes Plasmin as well as Plasminogen and

its activators t-PA and u-PA.

Glossary Text

Fibrinopeptide Fibrinopeptides are short amino acid sequences located on the

soluble fibrinogen molecule.

Fibrinthrombus Net of fibrin polymers, platelets, red and white blood cells to seal the

area of vessel wall damage.

Fibroblasts Fibroblasts synthesising the extracellular matrix and collagen, the

stroma for animal tissues, and plays an essential role in wound

healing.

Fibronectin Fibronectin is a protein found in plasma and on cell surfaces. It has

an important function in cell adhesion and can bind a wide variety of

molecules. In fibrin formation, fibronectin is both absorbed by fibrin

and bound to fibrin by Factor XIIIa-mediated cross-linking. The

normal range of fibronectin is between 150 - 720 mg / L and it is

mainly formed in the liver, the endothelium and fibroblasts.

Glycoprotein Substances, consisting of a protein and carbohydrate group.

GPIbα Glycoprotein Ibα. Receptor of vWF on the surface of platelets.

GPIIb / IIIa The glycoprotein IIb/IIIa complex is the receptor for fibrinogen and

Von Willebrand Factor. Fibrinogen binds to this receptor at the

surface of the platelets, allowing a robust gluing of the platelets.

GPIIIa Part of the Integrin α2bβ3 (GPIIb/IIIa) complex. Receptor of

Fibrinogen located on the platelet membrane.

Haemophilia Disease characterised by the partial or complete absence of a

coagulation factor. Most common haemophilia is Haemophilia A

(Factor VIII) followed by Haemophilia B (Factor IX).

Haemophilia A Disease characterised by the partial or complete absence of Factor

VIII. This x-chromosomal recessive inherited disease affects male

individuals while female individuals appearing as carrier.

Hageman factor Hageman factor. Serine protease activating Factor XI to Factor XIa

and Factor VII to Factor VIIa. Synthesised in the liver, Factor XIIa

under physiological conditions is present in blood at concentrations

at 70 - 120 %, but might show individual variances.

Glossary Text

HMWK High Molecular Weight Kininogen. HMWK is a α2-Globuline and also

called a contact factor and binds to negatively charged surfaces e.g.

platelets or endothelial cells where it binds Prekallekrein and Factor

XI. HMWK is synthesised in the liver and under physiological

conditions is present in blood at concentrations at approx. 80 mg/L.

High molecular weight

kininogen

HMWK for short. HMWK is a α2-Globuline and also called a contact

factor and binds to negatively charged surfaces e.g. platelets or

endothelial cells where it binds Prekallekrein and Factor XI. HMWK

is synthesised in the liver and under physiological conditions it is

present in the blood at concentrations at approx. 80 mg/L.

Inhibitor An agent or a substance stopping or blocking the activity of its

substrate.

Initiation Start of the plasmatic coagulation in the cell-based coagulation

model.

Intrinsic tenase

complex

Complex of coagulation factors activating the coagulation Factor X.

Kallikrein Contact factor of the coagulations activating Factor XII. The pro-

enzyme of Kallikrein is Prekallikrein activated by Factor XIIa in

presence of HMWK. Kallikrein is able to cleave Plasminogen and

Urokinase.

Kaolin Negatively charged substance situated in platelet granular.

Laminin Laminin is a glycoprotein and an essential component of the basal

membrane. It is of great importance for cell adhesion.

P2X1 Platelet P2X1 receptors generate increases in platelets Ca++,

causing the change of the platelet shape, movement of granules and

activation low levels of GPIIb/ IIIa. P2X1 activation by ATP released

from dense granules increases the aggregation responses to low

levels of the major agonists, collagen and Thrombin.

P2Y1 P2Y1 is a receptor at the platelet membrane. ADP binds to P2Y1

leading to mobilisation of Ca++ and subsequently to a change of the

platelet shape and platelet aggregation.

Glossary Text

P2Y12 P2Y12 is a receptor at the platelet membrane. ADP binds to P2Y12

leading to mobilisation of Ca++ and subsequently to a change of the

platelet shape and platelet aggregation.

PAI-1 Plasminogen Activator Inhibitor-1 prevents the dissolution of fibrin

clots.

PAR The protease activated Receptor is a G-coupled receptor located at

the surface of the platelets, endothelium and muscle cells. The PAR

is activated by cleavage of parts of their extracellular domain.

Currently four types of PAR are known: PAR-1, PAR-2, PAR-3 and

PAR-4. PARs activated by Thrombin (PAR-1, PAR-3 and PAR-4) on

the surface of platelets contributes to the activation of platelets.

Furthermore, PARs contribute to the regulation of vascular tone and

permeability, as well as inflammatory responses.

Phospholipids Phospholipids are a class of lipids and a major component of all cell

membranes. Phospholipids form lipid bilayers as a consequence of

their amphiphilic characteristics. The molecular structure of

phospholipids contains two hydrophobic fatty acids and a hydrophilic

phosphate group.

PL Phospholipids are a class of lipids and a major component of all cell

membranes. Phospholipids form lipid bilayers as a consequence of

their amphiphilic characteristic. The molecular structure of

phospholipids contains two hydrophobic fatty acids and a hydrophilic

phosphate group.

Plasmin Serine protease cleaving fibrin net into the water-soluble fibrin

degradation products. Plasmin interacts also with Factor V,

Fibrinogen and Factor VIII. Plasmin is activated mainly from

Plasminogen by t-PA and u-PA.

Glossary Text

Platelet Platelets are part of the non-liquid components of the blood.

Platelets in rest form round discs with a diameter of about 2-3 µm.

Under physiological conditions, they circulate close to the endothelial

wall without reacting with each other. In its membrane are inclusions

(granules) which, among other things, contains coagulation factors.

Damage to the endothelial layer causes adhesion and aggregation of

the platelets in the area of endothelial damage. Platelets play a

central role in primary coagulation. The normal range of platelets is

140,000-345,000 / µl. Reduced platelet counts are associated with

an increased risk of bleeding, but can be also be a sign of an

increased thrombosis risk (HIT-II).

Post-translational modification

Is the modification of proteins.

Prasugrel Drug, inhibiting irreversibly the ADP receptor P2Y12.

Proaccelerin Also Factor V. Factor V is the inactive form of coagulation Factor Va

and is activated by Thrombin (Factor IIa). Factor Va together with

Factor Xa forms the prothrombinase complex (together with Ca++

and phospholipids), with Factor Va acting as a cofactor. By

complexing with Factor Xa, the activation of Thrombin is accelerated

a thousand fold. Factor V is synthesised in the liver and is present in

plasma at a concentration of 60-150%. The most important inhibitor

of Factor Va is the Protein C / Protein S complex system. The

inability of the activated Protein C to cleave the Factor Va leads to

an increased risk of thrombosis (APC resistance, Factor V Leiden).

Proconvertin Factor VII. Vitamin-K depending pro-enzyme of the serine protease

Factor VIIa. Factor VIIa activates the coagulation Factors IX, X, VII,

II (Prothrombin) and X mostly in a complex with Tissue Factor.

Factor VII is synthesised in the liver and under physiological

conditions it is present in the blood at concentrations of 60 - 170 %.

Protein C/S system Complex of Protein C and Protein S to inhibit the coagulation

Cofactors Va and VIIIa.

Proteolysis Proteolysis is the enzymatic hydrolysis of proteins.

Glossary Text

Proteolytic cleavage

Describes in haemostasis the cleavage of an inactive form of a

coagulation factor resulting in the factor becoming active. The

cleavage induces a change in the conformity leading to the

availability of the active site of the enzyme for its substrate.

Prothrombin Factor II for short. Vitamin-K dependent pro-enzyme of the serine

protease Thrombin. Thrombin (= Factor IIa) is a central component

of plasmatic coagulation and reaction partner of a variety of

substrates. Under physiological conditions, Thrombin will not be

found in free form in the bloodstream. Prothrombin is synthesised in

the liver.

Prothrombinase Complex of coagulation factors activating the coagulation Factor II

(Prothrombin) to Factor IIa (Thrombin). The complex is formed by

Factor Xa, Factor Va, Ca++ and Phospholipids.

Prothrombinase

complex

Complex of coagulation Factors activating the coagulation Factor II

(Prothrombin) to Factor IIa (Thrombin). The complex is formed by

Factor Xa, Factor Va, Ca++ and Phospholipids.

Pseudopod Pseudopods are thin, variable plasma bulges of mobile body cells.

They are also present at protozoa.

Rivaroxaban Drug which belongs to a group of Direct Oral AntiCoagulants

inhibiting Factor Xa directly.

Rosenthal-factor Factor XI. Pro-enzyme (zymogen) of the serine protease Factor XIa

which activates Factor IX to Factor IXa is synthesised in the liver and

under physiological conditions is present in blood at concentrations

at 70 - 120 %.

Serin protease Are a group of enzymes that cleave peptides in proteins. The amino

acid serves here as the amino acid at the active site.

Serotonin Serotonin is carried by platelets (dense bodies) and released into the

plasma upon their activation. The vasoconstriction (constriction of

the vessel walls) induced by serotonin reduces the blood loss.

Furthermore, serotonin enhances the platelet aggregation triggered

by Thrombin and ADP.

Glossary Text

Shear rate Describes in liquids the spatial change of the flow velocity. Since

friction forces are present in real fluids, shearing of a fluid, just as in

the case of a solid, means a transmission of force.

Stuart-Prower-factor Factor X/ Factor Xa. Vitamin-K dependent serine protease activating

Factor II (Prothrombin) to Factor IIa (Thrombin) in the

prothrombinase complex with Cofactor Va, Ca++ and phosphlipids.

t-PA Tissue Plasminogen Activator is a protein catalysing the conversion

of Plasminogen to Plasmin.

TAFI Thrombin Activatable Fibrinolysis Inhibitor. Activated by high

concentrations of Thrombin stabilises TAFI the fibrin net and

prevents plasminogen and t-PA from binding to Fibrin.

TF, Tissue Factor Also known as Factor III. Protein of the cell membrane activates

Factor VII to Factor VIIa after its release into the blood due to cell

damage. Tissue Factor doesn't need to be activated.

Thrombin Thrombin (= Factor IIa) is a central component of plasmatic

coagulation and reaction partner of a variety of substrates. Under

physiological conditions, Thrombin will not be found in free form in

the bloodstream. The inactive form of Thrombin is Prothrombin

(Factor II), which is synthesised in the liver. Thrombin activates a

number of coagulation factors, is a potent platelet activator, and

activates the antithrombotic system. Thrombin acts on the fibrinogen

and cleaves the fibrinopeptides A and B from the fibrinogen

molecule, causing the polymerisation of the fibrinogen and forming

the fibrin web.

Tissue plasminogen

activator

t-PA for short. Converts Plasminogen to Plasmin. T-PA is

synthesised in endothelial cells and circulates in blood in active form

at concentrations at 5 µg/l.

Thrombin-Activatable

Fibrinolysis-Inhibitor

TAFI. Activated by high concentrations of Thrombin TAFI stabilises

the fibrin net and prevents plasminogen and t-PA from binding to

fibrin.

Glossary Text

Thrombokinase Stuard-Prower Factor or Factor Xa. Vitamin-K dependent serine

protease activating Factor II (Prothrombin) to Factor Iia (Thrombin) in

the prothrombinase complex with Cofactor Va, Ca++ and

phospholipids.

Thrombomodulin Protein located on the surface of the endothelial cells serving as a

cofactor of Thrombin. Thrombomoduline modifies Thrombin from a

pro-coagulant to an anti-coagulant enzyme.

Thromboxan A2 TXA 2 for short, occurs mainly in the platelets and is the product of

thromboxane synthesis, which results from the cyclooxygenase

mediated conversion of arachidonic acid. It belongs to the group of

prostaglandins and activates platelet aggregation via its receptor.

Thrombus Net of fibrin polymers, platelets, red and white blood cells to seal the

area of vessel wall damage.

TXA2 Thromboxane A2 occurs mainly in the platelets and is the product of

thromboxane synthesis, which results from the cyclooxygenase

mediated conversion of the arachidonic acid. It belongs to the group

of prostaglandins and activates platelet aggregation via its receptor.

u-PA urokinase-type Plasminogen Activator is a protein catalysing the

conversion of Plasminogen to Plasmin.

Vitamin-K antagonists A group of drugs that inhibit blood clot formation. The various active

ingredients can be taken as a tablet and are usually effective after

two to three days, while the effect persists after weaning up to 5

days. The most common Vitamin-K antagonists are Warfarin,

Marcumar and Falithrom.

Glossary Text

vWF Von Willebrand Factor is an adhesive protein that circulates in the

blood. It binds the platelets to the injured endothelial wall (=

subendothelium), connects platelets to each other, and binds

circulating Factor VIII, preventing the Factor VIII from prematurely

breaking down. It therefore occupies a key position in primary and

plasmatic haemostasis. Von Willebrand Factor is synthesised in the

endothelial cells and megakaryocytes. Its normal range is very broad

and depends on various factors such as e.g. the blood type. The

intraindividual fluctuations can also be very high (CV up to 40%).

Generally, without consideration of the blood group, a normal range

of 40 - 240% is given.

vWR Receptor at the platelet membrane for von Willebrand Factor. VWF

bound to vWR facilitates the platelet adhesion to subendothelial cells

after vessel wall damage and contributes to the platelet activation.