...................blood clotting???

Question

how does the blood knows that there is an injury and the blood should start clotting also if heparin is present in blood then hoe does it clots????

Answer 1

I (fibrinogen) Forms clot (fibrin)

II (prothrombin) Its active form (IIa) activates I, V, VIII, XI, XIII, protein C, platelets

Tissue factor Co-factor of VIIa (formerly known as factor III)

Calcium Required for coagulation factors to bind to phospholipid (formerly known as factor IV)

V (proaccelerin, labile factor) Co-factor of X with which it forms the prothrombinase complex

VI Unassigned – old name of Factor Va

VII (stable factor) Activates IX, X

VIII (antihemophilic factor) Co-factor of IX with which it forms the tenase complex

IX (Christmas factor) Activates X: forms tenase complex with factor VIII

X (Stuart-Prower factor) Activates II: forms prothrombinase complex with factor V

XI (plasma thromboplastin antecedent) Activates IX

XII (Hageman factor) Activates factor XI and prekallikrein

XIII (fibrin-stabilizing factor) Crosslinks fibrin

von Willebrand factor Binds to VIII, mediates platelet adhesion

prekallikrein Activates XII and prekallikrein; cleaves HMWK

high molecular weight kininogen (HMWK) Supports reciprocal activation of XII, XI, and prekallikrein

fibronectin Mediates cell adhesion

antithrombin III Inhibits IIa, Xa, and other proteases;

heparin cofactor II Inhibits IIa, cofactor for heparin and dermatan sulfate ("minor antithrombin")

protein C Inactivates Va and VIIIa

protein S Cofactor for activated protein C (APC, inactive when bound to C4b-binding protein)

protein Z Mediates thrombin adhesion to phospholipids and stimulates degradation of factor X by ZPI

Protein Z-related protease inhibitor (ZPI) Degrades factors X (in presence of protein Z) and XI (independently)

plasminogen Converts to plasmin, lyses fibrin and other proteins

alpha 2-antiplasmin Inhibits plasmin

tissue plasminogen activator (tPA) Activates plasminogen

urokinase Activates plasminogen

plasminogen activator inhibitor-1 (PAI1) Inactivates tPA & urokinase (endothelial PAI)

plasminogen activator inhibitor-2 (PAI2) Inactivates tPA & urokinase (placental PAI)

cancer procoagulant Pathological factor X activator linked to thrombosis in cancer

Answer 2

Simply put, if a blood vessel is cut, the blood plasma (which contains water, salt and proteins, but doesn't have cells or platelets) is exposed to tissue around the blood vessel and this causes blood proteins and platelets to form a clot.

The more complicated version is that the tissue around the blood vessel (the subendothelium) contains a protein called Tissue Factor (actually it is a glycoprotein, also known as Factor III) which stimulates several proteins in the plasma to start forming a clot.  At the same time, platelets are activated and begin to stick at the site of the blood vessel injury.  The plasma proteins work together to form a meshwork around the platelets.  The main plasma proteins are Factor VII, Factor X, prothrombin and fibrinogen, each of which exist in the blood plasma in an inactive form (those are Roman Numerals).  The activated forms are proteases (specifically serine proteases), which cut specific proteins.  When Factor VII is exposed to Tissue Factor, it is activated into Factor VIIa which cuts the protein Factor X and activates it into Factor Xa, which cuts the protein prothrombin into two pieces (thus activating prothrombin), one of which is called thrombin, and then fibrinogen is cut by thrombin into smaller pieces called fibrin.  The meshwork around the platelets is composed of the protein called fibrin.  The platelets and fibrin meshwork stops the blood from escaping the severed blood vessel until the cells in the blood vessel wall can start growing and fix the blood vessel.  So, it is a pretty neat system, the blood plasma isn't activated to form a clot unless it comes in contact with Tissue Factor and that won't happen unless the blood vessel is cut which allows the plasma and Tissue Factor to interact.  If you look this up, it is called the Extrinsic Pathway for blood coagulation.  As you can guess, if the cut is too severe, this process won't fix the cut and the bleeding will continue.

Note that there are other ways for the plasma proteins to start forming a clot (called the Intrinsic Pathway), which may have some significance to clots forming when there is no exposure to tissue factor.

As for heparin (an anti-coagulant or "blood thinner"), it prevents blood from clotting by interfering with the coagulation cascade (it interferes with Factor Xa and thrombin).  When heparin (or other anti-coagulants like Coumadin/Warfarin) are given, we test and test to make sure we give enough to treat the problem, but not too much in order to make sure that we allow the blood to clot if it really needs to.

As a side note, exposure of blood to air does not cause blood to clot.  That is an older thought and it is now known that, instead of air, it was the container blood was placed in (especially if it is glass) that caused activation of the clotting cascade.  Adding a good anticoagulant to bloood will prevent blood from clotting even if the blood is left exposed to air.

Answer 3

When blood vessels are cut or damaged, the loss of blood from the system must be stopped before shock and possible death occur. This is accomplished by solidification of the blood, a process called coagulation or clotting.

A blood clot consists of

a plug of platelets enmeshed in a

network of insoluble fibrin molecules.

Platelet aggregation and fibrin formation both require the proteolytic enzyme thrombin. Clotting also requires:

calcium ions (Ca2+)(which is why blood banks use a chelating agent to bind the calcium in donated blood so the blood will not clot in the bag).

about a dozen other protein clotting factors. Most of these circulate in the blood as inactive precursors. They are activated by proteolytic cleavage becoming, in turn, active proteases for other factors in the system.

By tradition, these factors are designated by Roman numerals. I find this somewhat confusing and will use Arabic numerals instead.

I hope u got ya answer

Answer 4

Blood clots are formed by the process of coagulation - the blood’s natural tendency to clump and plug an injured blood vessel. Blood clots are made of blood cells and fibrin strands. They serve a valuable function in wound healing and stopping the flow of blood after an injury.

For example, when a person is cut, blood flows from the injured blood vessel for a short period. However, the clotting process begins almost immediately.

During this process, blood platelets first gather at the site of the injury and form a loose plug. These platelets release a number of chemicals that enhance and promote blood clotting. Once the loose platelet plug is in place, a mesh of fibrin forms to create a stronger blood clot. This blood clot will remain in place as the tissue injury heals.

After it heals, still other chemicals are responsible for dissolving the clot. This process of forming and dissolving blood clots is called hemostasis.

Answer 5

well

Coagulation is a complex process by which blood forms clots. It is an important part of hemostasis (the cessation of blood loss from a damaged vessel) whereby a damaged blood vessel wall is covered by a platelet and fibrin containing clot to stop bleeding and begin repair of the damaged vessel. Disorders of coagulation can lead to an increased risk of bleeding (hemorrhage) and/or clotting (thrombosis).

Coagulation is highly conserved throughout biology; in all mammals, coagulation involves both a cellular (platelet) and a protein (coagulation factor) component. The system in humans has been the most extensively researched and therefore is the best understood.

Coagulation is initiated almost instantly after an injury to the blood vessel damages the endothelium (lining of the vessel). Platelets immediately form a hemostatic plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously; proteins in the blood plasma, called coagulation factors, respond in a complex cascade to form fibrin strands which strengthen the platelet plug.

Damage to blood vessel walls exposes subendothelium proteins, most notably collagen, present under the endothelium. Circulating platelets bind collagen with surface collagen-specific glycoprotein Ia/IIa receptors. The adhesion is strengthened further by the large, multimeric circulating proteins von Willebrand factor (vWF), which forms links between the platelets glycoprotein Ib/IX/V and the collagen fibrils. This adhesion activates the platelets.

Activated platelets release the contents of stored granules into the blood plasma. The granules include ADP, serotonin, platelet activating factor (PAF), vWF, platelet factor 4 and thromboxane A2 (TXA2) which in turn activate additional platelets. The granules contents activate a Gq-linked protein receptor cascade resulting in increased calcium concentration in the platelets' cytosol. The calcium activates protein kinase C which in turn activates phospholipase A2 (PLA2). PLA2 then modifies the integrin membrane glycoprotein IIb/IIIa, increasing its affinity to bind fibrinogen. The activated platelets changed shape from spherical to stellate and the fibrinogen cross-links with glycoprotein IIb/IIIa aid in aggregation of adjacent platelets.

The coagulation cascade of secondary hemostasis has two pathways, the contact activation pathway (formerly known as the intrinsic pathway) and the tissue factor pathway (formerly known as the extrinsic pathway) that lead to fibrin formation. It was previously thought that the coagulation cascade consisted of two pathways of equal importance joined to a common pathway. It is now known that the primary pathway for the initiation of blood coagulation is the tissue factor pathway. The pathways are a series of reactions, in which a zymogen (inactive enzyme precursor) of a serine protease and its glycoprotein co-factor are activated to become active components that then catalyze the next reaction in the cascade, ultimately resulting in cross-linked fibrin. Coagulation factors are generally indicated by Roman numerals, with a lowercase a appended to indicate an active form.

The coagulation factors are generally serine proteases (enzymes). There are some exceptions. For example, FVIII and FV are glycoproteins and Factor XIII is a transglutaminase. Serine proteases act by cleaving other proteins at specific sites. The coagulation factors circulate as inactive zymogens.

The coagulation cascade is classically divided into three pathways. The tissue factor and contact activation pathways both activate the "final common pathway" of factor X, thrombin and fibrin.

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Answer 6

Blood clots due to a number of factors. These include exposure to air, but also the damaged cells from the wound. These factors, and more of them, trigger a chain reaction that converts fibrinogen, a soluble protein, into insoluble fibrin, that forms a network trapping blood, which shrinks and forms a scab.

Heparin prevents clotting for a certain amount of time. It allows the wound to bleed, flushing out toxins and contaminants such as bacteria that could cause wound infections. However, the heparin is also flushed out at some point, so the blood can start to clot.