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Blood clotting mechanism

Posted by Mumtaz khan Friday, 21 October 2011 0 comments

        Clotting is a much complex process in which all the coagulation factor must synchronize and activate each other.Basically the entire mechanism of clotting can be explained in 3 steps.
1. Formation of Prothombinase .
2. Conversion of plasma protein-prothombin into an enzyme called Thrombin by the activator-Prothombinase.
3. Conversion of another plasma protein called Fibrinogen which is soluble,into insoluble Fibrin under the influence of Thrombin.

The extrinsic pathway of blood clotting has few steps as compared to the intrinsic pathway .This is because of clotting comes into play.When there is a severe trauma and occurs rapidly.It has been named Extrinsic because a tissue factor which is a tissue protein i.e.,coagulation factor III popularly referred as Thromboplastin leaks into the blood from the tissue cells which are outside the blood vessels(so extrinsic).This coagulation factor III is a complex mixture of Lipoprotein and phospholipid which gets released from the surface of damaged cells.Since the factor is released from the site of injury itself the 3 stage process of clotting will be rapid.This Thromboplastin activates coagulation factor VII in presence of Calcium ions.Coagulation factor VII gets activated w+hich again in the presence of Calcium ions activates CF X.Once CF X is activated it combines w+ithCF V again in the presence of Calcium ions form active enzyme Prothombinase.Formation of Prothombinase satisfies the 1st stage process in blood clotting.
Stage 2 and stage 3 processes i.e.,conversion of plasma protein Prothrombin into enzyme Thrombin by using prothrombinase and finally conversion of soluble plasma proteins fibrinogen into insoluble threads fibrin by using thrombin are the next steps completing the Extrinsic pathway.

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Coagulation of blood

Posted by Mumtaz khan Monday, 17 October 2011 0 comments

Homeostasis refers to stoppage of bleeding.when blood vessels are ruptured or damaged hemostatic response must be quick localised to the region of damage and carefully controlled three basic mechanisms present blood loss viz,
(1) Vascular spasm.
When the blood vessels are damaged the circularly arranged smooth muscles immediately contracts this is referred to as vascular spasm and will reduce blood loss.This is crucial because during this time other homeostatic mechanism get into operation.The vascular spasm is caused by damage to the smooth muscles and reflexes initiated by pain receptors.

(2) Platelet plug formation.
The blood platelets in their original unstimulated state are disc shaped showing two types of granules in their cytoplasm viz., alpha granules and dense granules.
In the first phase of platelet formation,blood platelet come together make a contact and stick to the part of damaged blood vessels.This process is called platelet adhesion.As a result of adhesion,the platelets which were earlier unstimulated now become activated and their charactreistics change drastically.They extend projections which help them to make further contacts with the neighboring platelets and to release  their contents from the granules.This is referred to as platelet release reaction.The liberated ATP will activate the neighboring platelets as well. Serotonin  alongwith a factor called thromboxane causes vasoconstriction.Thus decreasing the bloodflow..The release of ADP will make the platelets more sticky and this stickiness will cause them to adhere to each other. This gathering of platelets for stickiness is referred to as Platelet Aggregation.

(3) Blood clotting.
 Normally blood remains in th liquid state as long as it stays within the blood vessels but if it is withdrawn from the body it gets converted from the fluid state into a gel state.Eventually the gel separates from the liquid and a yellow colored or straw colored liquid which oozes out from blood clot,is called Serum(Serum means plasma clotting proteins). The remaining gel is called a clot consisting of network of insoluble fibers of fibrin in which blood corpuscles get trapped.This process of gel formation is called coagulation or clotting.
    Clotting involves several enzymes and other chemicals known as Clotting factors.Most of these clotting factors are synthesized in the liver and finally released in the blood plasma.There are some clotting factors which is released by blood platelets and some clotting factor (recently accepted)which is released from the damaged tissue cells earlier it was called as Thromboplastin.

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Posted by Mumtaz khan Monday, 10 October 2011 0 comments

         Hemoglobin is the major oxygen carrying molecule was the first oligomeric protein to be studied by X- ray diffraction methods.

         Two major types of hemoglobin occur in humans at different stages of development namely,Feotal Hemoglobin(Hb F),and Adult hemoglobin(Hb A). Other forms of hemoglobin such as embryonic and minor adult forms do exist.
        Each molecule of hemoglobin is composed of four polypeptide chains plus a heam group.hemoglobin A contains two identical alpha chains and two identical beta-chains.There is another type of hemoglobin A which contains sigma chains.
        Before birth several additional hemoglobin polypeptides are synthesized e.g., In early embryonic life hemoglobin show presence of Epsilon chain while in the fetal life it shows the presence of two alpha chains.While in the fetal life it shows the presence of two alpha chains and two sigma chains because both hemoglobin in embryonic life and hemoglobin in fetal life have grater affinity for oxygen than hemoglobin in adult life.The feotus can prefentially absorb from maternal blood streams.
       Each peptide chain whether alpha,beta or sigma is encoded by a specific gene.Hb F present in developing feotus is normally replaced by Hb Awithin the 1st 6 monthsafter birth.Each polypeptide consists of specific sequence of a specific sequence of AA's.

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