Glossary: Basics of Haemostasis Online Training

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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.

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Transcript of Glossary: Basics of Haemostasis Online Training

Microsoft Word - Glossary_final.docxGlossary Text
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.
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
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 %.
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
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 2bβ3 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.
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).
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.
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.
(Prothrombin) to Factor IIa (Thrombin). The complex is formed by
Factor Xa, Factor Va, Ca++ and Phospholipids.
Prothrombinase
complex
(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.
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.
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.
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