Category Archives: Physiology of blood clotting

Physiology of blood clotting

Blood is a necessary component of the human body, and the loss of this fluid may be life-threatening. The human body protects against loss of blood through the clotting mechanism. Through vasoconstriction, adhesion, activation, and aggregation, the contributors form a transient plug to act as the cork to the leaking blood flow. Soon after, fibrin, the functioning form of fibrinogen, stabilizes this weak platelet plug. The scope of this article will highlight the physiological aspects of the clotting mechanism.

The cellular components of the clotting mechanism include platelets, endothelial cells, and a series of proteins, enzymes, and ions. The clotting mechanism involves the circulatory system which includes the lineage of blood cells and blood vessels.

The clotting mechanism is broken into 2 stages: [4] [5] [6]. Vasospasm of the blood vessels occurs first in response to injury of the vasculature.

This vasospasm, in turn, stimulates vasoconstriction. Vasoconstriction is primarily mediated by endothelin-1, a potent vasoconstrictor, which is synthesized by the damaged endothelium. Damaged endothelium exposes sub-endothelial collagen, von Willebrand factor vWFreleases ATP, and inflammatory mediators.

Weibel-Palade bodies of the endothelium also synthesize vWF.

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It is the combination of exposure of vWF, subendothelial collagen, ATP, and inflammatory mediators which provide the gateway into the second phase of primary hemostasis, platelet adhesion. Post vascular damage, platelets begin to roll along vessel walls and adhere to areas of exposed subendothelial collagen and vWF. Platelet membranes are rich in G protein Gp receptors located within the phospholipid bilayer.

Specifically, it is Gp Ib-IX receptor on platelets that bind to vWF within the endothelium that creates the initial connection between the two. Once bound, a variety of events can occur in the third phase of primary hemostasis to activate the platelet. First, platelets will undergo an irreversible change in shape from smooth discs to multi-pseudopodal plugs, which greatly increases their surface area.

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Second, platelets secrete their cytoplasmic granules. Thrombin directly activates platelets via proteolytic cleavage by binding the protease-activated receptor. Thrombin also stimulates platelet granule release which includes serotonin, platelet activating factor, and Adenosine Diphosphate ADP. ADP is an important physiological agonist which is stored specifically in the dense granules of platelets. P2Y1 induces the pseudopod shape change and aids in platelet aggregation.

P2Y12 plays a major role in inducing the clotting cascade.Breakage of the endothelial lining of a vessel exposes collagen proteins from the subendothelial connective tissue to the blood. This initiates three separate, but overlapping, hemostatic mechanisms: 1 vasoconstriction, 2 the formation of a platelet plugand 3 the production of a web of fibrin proteins that penetrates and surrounds the platelet plug. In the absence of vessel damage, platelets are repelled from each other and from the endothelial lining of vessels.

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The repulsion of platelets from an intact endothelium is believed to be due to prostacyclin, a type of prostaglandin see chapter 11, fig.

Mechanisms that prevent platelets from sticking to the blood vessels and to each other are obviously needed to prevent inappropriate blood clotting. Damage to the endothelium of vessels exposes subendothelial tissue to the blood. Platelets are able to stick to exposed collagen proteins that have become coated with a protein von Willebrand factor secreted by endothelial cells.

Platelets contain secretory granules; when platelets stick to collagen, they degranulate as the secretory granules release their products. These products include adenosine diphosphate ADPserotonin, and a prostaglandin called thromboxane A2.

physiology of blood clotting

This event is known as the platelet release reaction. Serotonin and thromboxane A2 stimulate vasoconstriction, which helps to decrease blood flow to the injured vessel. Phos-pholipids that are exposed on the platelet membrane participate in the activation of clotting factors.

The release of ADP and thromboxane A2 from platelets that are stuck to exposed collagen makes other platelets in the vicinity "sticky," so that they adhere to those stuck to the collagen. The second layer of platelets, in turn, undergoes a platelet release reaction, and the ADP and thromboxane A2 that are secreted cause additional platelets to aggregate at the site of injury. This produces a platelet plug in the damaged vessel, which is strengthened by the activation of plasma clotting factors.

In order to undergo a release reaction, the platelets must produce prostaglandins. Since platelets lack nuclei and are not complete cells, they cannot regenerate new enzymes. Therefore, the enzymes remain inhibited for the life of the platelets. The ingestion of excessive amounts of aspirin can thus significantly prolong bleeding time for several days, which is why blood donors and women in the last trimester of pregnancy are advised to avoid aspirin.

physiology of blood clotting

Slight inhibition of platelet aggregation by low doses of aspirin, however, can reduce the risk of atherosclerotic heart diseaseand such a regimen is often recommended for patients diagnosed with this condition. The platelet plug is strengthened by a meshwork of insoluble protein fibers known as fibrin fig. Blood clots therefore contain platelets and fibrin, and they usually contain trapped red blood cells that give the clot a red color clots formed in arteries, where the blood flow is more rapid, generally lack red blood cells and thus appear gray.

Finally, contraction of the platelet mass in the process of clot retraction forms a more compact and effective plug. Fluid squeezed from the clot as it retracts is called serum, which is plasma without fibrinogen, the soluble precursor of fibrin. Serum is obtained in laboratories by allowing blood to clot in a test tube and then centrifuging the tube so that the clot and blood cells become packed at the bottom of the tube.

The conversion of fibrinogen into fibrin may occur via either of two pathways. Blood left in a test tube will clot without. Heart and Circulation the addition of any external chemicals; the pathway that produces this clot is thus called the intrinsic pathway.

The intrinsic pathway also produces clots in damaged blood vessels when collagen is exposed to plasma. Damaged tissues, however, release a chemical that initiates a "shortcut" to the formation of fibrin.

Since this chemical is not part of blood, the shorter pathway is called the extrinsic pathway. The intrinsic pathway is initiated by the exposure of plasma to a negatively charged surface, such as that provided by collagen at the site of a wound or by the glass of a test tube.

This activates a plasma protein called factor XII table Active factor XII in turn activates another clotting factor, which activates yet another.The primary function of blood is to supply oxygen and nutrients as well as constitutional elements to tissues and to remove waste products.

Blood also enables hormones and other substances to be transported between tissues and organs. Problems with blood composition or circulation can lead to downstream tissue malfunction. Blood is also involved in maintaining homeostasis by acting as a medium for transferring heat to the skin and by acting as a buffer system for bodily pH. The blood is circulated through the lungs and body by the pumping action of the heart. The right ventricle pressurizes the blood to send it through the capillaries of the lungs, while the left ventricle re-pressurizes the blood to send it throughout the body.

Pressure is essentially lost in the capillaries, hence gravity and especially the actions of skeletal muscles are needed to return the blood to the heart. Oxygen O 2 is the most immediate need of every cell and is carried throughout the body by the blood circulation.

Oxygen is used at the cellular level as the final electron acceptor in the electron transport chain the primary method of generating ATP for cellular reactions. Oxygen is carried in the blood bound to hemoglobin molecules within red blood cells. Hemoglobin binds oxygen when passing through the alveoli of the lungs and releases oxygen in the warmer, more acidic environment of bodily tissues, via simple diffusion.

Carbon dioxide CO 2 is removed from tissues by blood and released into the air via the lungs. Carbon dioxide is produced by cells as they undergo the processes of cellular respiration particularly the Kreb's Cycle. The molecules are produced from carbons that were originally part of glucose. Most of the carbon dioxide combines with water and is carried in the plasma as bicarbonate ions. An excess of carbon dioxide through exercise, or from holding ones breath quickly shifts the blood pH to being more acidic acidosis.

Chemoreceptors in the brain and major blood vessels detect this shift and stimulate the breathing center of the brain the medulla oblongata. Hence, as CO 2 levels build up and the blood becomes more acidic, we involuntarily breathe faster, thus lowering CO 2 levels and stabilizing blood pH. In contrast, a person who is hyperventilating such as during a panic attack will expire more CO 2 than being produced in the body and the blood will become too alkaline alkalosis.

Blood is a circulating tissue composed of fluid plasma and cells red blood cells, white blood cells, platelets. Anatomically, blood is considered a connective tissue, due to its origin in the bones and its function.

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Blood is the means and transport system of the body used in carrying elements e. One percent of the plasma is salt, which helps with the pH of the blood. The largest group of solutes in plasma contains three important proteins to be discussed. There are: albuminsglobulinsand clotting proteins. They are produced in the liver. The main function of albumins is to maintain the osmotic balance between the blood and tissue fluids and is called colloid osmotic pressure.

In addition, albumins assist in transport of different materials, such as vitamins and certain molecules and drugs e.

Globulins are a diverse group of proteins, designated into three groups: gamma, alpha, and beta. Their main function is to transport various substances in the blood. Gamma globulins assist the body's immune system in defense against infections and illness. Clotting proteins are mainly produced in the liver as well. There are at least 12 substances, known as "clotting factors" that participate in the clotting process.Basic Theory. More than 50 important substances that cause or affect blood coagulation have been found in the blood and in the tissues—some that promote coagulation, called procoagulants, and others that inhibit coagulation, called anticoagulants.

Whether blood will coagulate depends on the balance between these two groups of substances. In the blood stream, the anticoagulants normally predominate, so that the blood does not coagulate while it is circulating in the blood vessels.

But when a vessel is ruptured, procoagulants from the area of tissue damage become "activated" and override the anticoagulants, and then a clot does develop. General Mechanism. All research workers in the field of blood coagulation agree that clotting takes place in. First, prothrombin activator is formed as a result of rupture of a blood vessel or as a result of damage to special substances in the blood. Third, the thrombin causes polymerization of fibrinogen molecules into fibrin fibers within another 10 to 15 seconds.

Thus, the rate-limiting factor in causing blood coagulation is usually the formation of prothrombin activator and not the subsequent reactions beyond that point, because these terminal steps normally occur rapidly to form the clot itself.

Platelets also play an important role in the conversion of prothrombin to thrombin because much of the prothrombin first attaches to prothrombin receptors on the platelets already bound to the damaged tissue. Prothrombin and Thrombin.

Prothrombin is a plasma protein, an alpha2-globulin, having a molecular weight of 68, It is an unstable protein that can split easily into smaller compounds, one of which is thrombin, which has a molecular weight of 33, almost exactly one half that of prothrombin. Prothrombin is formed continually by the liver, and it is continually being used throughout the body for blood clotting. If the liver fails to produce prothrom-bin, in a day or so prothrombin concentration in the plasma falls too low to provide normal blood coagulation.

Vitamin K is required by the liver for normal formation of prothrombin as well as for formation of a few other clotting factors. Therefore, either lack of vitamin K or the presence of liver disease that prevents normal prothrombin formation can decrease the prothrombin level so low that a bleeding tendency results. Fibrinogen is formed in the liver, and liver disease can decrease the concentration of circulating fibrinogen, as it does the concentration of prothrombin, pointed out above.

Because of its large molecular size, little fibrinogen normally leaks from the blood vessels into the interstitial fluids, and because fibrinogen is one of the essential factors in the coagulation process, interstitial fluids ordinarily do not coagulate. Yet, when the permeability of the capillaries becomes pathologically increased, fibrinogen does then leak into the tissue fluids in sufficient quantities to allow clotting of these fluids in much the same way that plasma and whole blood can clot.

Action of Thrombin on Fibrinogen to Form Fibrin. Thrombin is a protein enzyme with weak proteolytic capabilities. It acts on fibrinogen to remove four low-molecular-weight peptides from each molecule of fibrinogen, forming one molecule of fibrin monomer that has the automatic capability to polymerize with other fibrin monomer molecules to form fibrin fibers.

Therefore, many fibrin monomer molecules polymerize within seconds into long fibrin fibers that constitute the retic-ulum of the blood clot.

Mechanism of Blood Coagulation

In the early stages of polymerization, the fibrin monomer molecules are held together by weak non-covalent hydrogen bonding, and the newly forming fibers are not cross-linked with one another; therefore, the resultant clot is weak and can be broken apart with ease. But another process occurs during the next few minutes that greatly strengthens the fibrin reticulum.

This involves a substance called fibrin-stabilizing factor that is present in small amounts in normal plasma globulins but is also released from platelets entrapped in the clot. Before fibrin-stabilizing factor can have an effect on the fibrin fibers, it must itself be activated.

The same thrombin that causes fibrin formation also activates the fibrin-stabilizing factor. Then this activated substance operates as an enzyme to cause covalent bonds between more and more of the fibrin monomer molecules, as well as multiple cross-linkages between adjacent fibrin fibers, thus adding tremendously to the three-dimensional strength of the fibrin meshwork.

Blood Clot. The clot is composed of a meshwork of fibrin fibers running in all directions and entrapping blood cells, platelets, and plasma.

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The fibrin fibers also adhere to damaged surfaces of blood vessels; therefore, the blood clot becomes adherent to any vascular opening and thereby prevents further blood loss. Clot Retraction—Serum. Within a few minutes after a clot is formed, it begins to contract and usually expresses most of the fluid from the clot within 20 to 60 minutes.

The fluid expressed is called serum because all its fibrinogen and most of the other clotting factors have been removed; in this way, serum differs from plasma.Blood Clotting is one of three mechanisms that reduce the loss of blood from broken blood vessels.

Human Physiology/Blood physiology

The smooth muscle in blood vessel walls contracts immediately the blood vessel is broken. This response reduces blood loss for some time, while the other haemostatic mechanisms become active. The key stages of this process are called platelet adhesion, platelet release reaction, and platelet aggregation. Following damage to a blood vessel, vascular spasm occurs to reduce blood loss while other mechanisms also take effect.

Blood platelets congregate at the site of damage and amass to form a platelet plug. Blood normally remains in its liquid state while it is within the blood vessels but when it leaves them the blood may thicken and form a gel coagulation.

This blood clotting is a complex process involving many clotting factors incl. This is initiated by liquid blood making contact with a foreign surface, i. Both the intrinsic and the extrinsic systems involve interactions between coagulation factors. These coagulation factors have individual names but are often referred to by a standardised set of Roman Numerals, e. Prothrombinase formed in stage 1. In turn, thrombin converts fibrinogen which is also a plasma protein synthesized in the liver into fibrin.

The intrinsic pathway, which is triggered by elements that lie within the blood inself intrinsic to the bloodoccurs in the flowing way. Damage to the vessel wall stimulates the activation of a cascade of clotting factors for the sake of simplicity we will not consider the individual factors. This cascade results in the activation of factor X.

physiology of blood clotting

Activated factor X is an enzyme that converts prothrombin to thrombin. Thrombin converts fibrinogen to fibrin monomers, which then polymerize in fibrin fibers. Fibirin fibers form a losse meshwork that is stabilized by crosslinks created by factor XIII. The stabilized meshwork of fibrin fibers ins now a clot that traps red blood cells and platelets and thus stops the flow of blood. The extrinsic pathway is triggered by tissue damage outside of the blood vessel. This pathway acts to clot blood that has escaped from the vessel into the tissues.

Damage to tissue stimulates the activation of tissue thromboplastin, an enzyme that catalyzed the activation of factor X.

At this point the intrinsic and extrinsic pathways converge and the subsequent steps are the same as those described above. With advanced atherosclerosis take one baby asprin yet day to reduce the probability of heart attack and stroke.

Small tears of the capillaries and arterioles are happening all the time Platelets are responsible for quickly sealing these tears before the slower process of clotting completes the job. In the absence of adequate numbers of platelets these micro blotches thrombocytopenia purpura visible on the skin. Thrombocytopenia can be acute or chronic and has many causes. Severe, untreated cases result in death. The blood contains about a dozen clotting factors.

These factors are proteins that exist in the blood in an inactive state, but can be called into action when tissues or blood vessels are damaged. The first factor in the sequence activates the second factor, which activates the third factors and so on. This series of reactions is called the clotting cascade. Blood clotting is the transformation of liquid blood into a semisolid gel.Note : The structure and function of the heart and other aspects of the vascular system is part of training in therapies such as massage incl.

Indian Head Massage, Swedish Massage, acupressure massage, aromatherapy, acupuncture, shiatsu, and others. This page is intended to include information suitable for most basic first level courses in these therapies, and some ITEC Diplomas. Blood Clotting is one of three mechanisms that reduce the loss of blood from broken blood vessels. Following damage to a blood vessel, vascular spasm occurs to reduce blood loss while other mechanisms also take effect:. Formation of Prothrombinase Prothrombinase can be formed in two ways, depending of which of two 'systems' or 'pathways' apply.

These are. Both the intrinsic and the extrinsic systems involve interactions between coagulation factors.

Blood Clotting

The coagulation factors have individual names but are often referred to by a standard set of Roman Numerals, e. This is blood clotting in an unbroken blood vessel, which is dangerous and can lead to strokes or heart-attacks. Conversely, if blood takes too long to clot hemorrhage may occur. In this case much blood may be lost from the blood vessels, which is also dangerous. The hereditary disorder haemophilia is a condition in which certain coagulation factors are missing from the blood, as a result of which the blood cannot form clots without medical intervention.

See also pages about the structure and functions of bloodblood vesselsblood pressurethe structure of the heartthe functions of the heartand the systemic circulation and the vascular system generally. Kale is in season in February - 7 Feb ' Reducing saturated fat in diet lowers blood cholesterol and risk of CVD - 1 Aug ' Benefits of interval training for vascular health of older women - 7 Aug ' Vet charity warning about pet obesity - 25 Mar ' Electrocardiogram ECG in ambulances save lives - 14 Apr ' Mediterranean diet linked with lower risk of heart disease - 4 Feb 'The Adobe Digital Insights 2017 Holiday Predictions Report and Holiday Actuals Report are based on aggregate and anonymized data via the Adobe Analytics and Adobe Experience Cloud.

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Contact us Powered by The Adobe Digital Insights 2017 Holiday Predictions Report and Holiday Actuals Report are based on aggregate and anonymized data via the Adobe Analytics and Adobe Experience Cloud. On Saturday at a sold out Theater at Madison Square Garden, dual Olympic champions Vasyl Lomachenko and Guillermo Rigondeaux go mano a mano for the formers WBO Super Feather strap.

It reminds me of Sugar Ray Leonard vs Marvin Hagler, two skilsters at the very highest level. Look how easily both have dealt with top opposition. Riga has much faster hands and being the bookies underdog might inspire him even more. Too big, too fast, too young. If he connects clean, I can even see him stopping Rigondeaux.

physiology of blood clotting

I think Rigondeaux wins a tight, thinking fight, rather than a physical fight. He showed holes that Rigondeaux can exploit. Rigondeaux never fights, always boxes. I see him draining the Cuban and then overwhelming him. Joseph Agbeko (ex two time IBF bantam champion) told me Rigondeaux punches brutally hard. Lomachenko already has one loss on his record and will lose again.

Blood Clotting: Mechanisms and Stages | Blood | Hematology | Biology

A good big fighter beats a good little fighter and Lomachenko could even stop him. I see him winning by stoppage somewhere around the eighth or ninth. He attacks from angles rather than straight lines. Rigondeaux is very patient on the back foot and has exceptional timing but I think Lomachenko will be too busy and too big physically. What a match up. No one has more ability than this pair. Both have got talent pouring out of their ears. Both have got great attributes and can win any fight on their best day.

Rigondeaux is the more experienced and very sharp. He might be able to catch Lomachenko and deliver the knockout blow. So, IOW, after the fight ends, there will either be 11 experts who are no longer experts, or 3 experts who are no longer experts. My head is spinning. And someone posted yesterday that around the time of the weigh-in, Vegas odds were 2. He's too good for him. Tags: Vasyl Lomachenko Guillermo Rigondeaux Lomachenko vs. Post a Comment - View More User Comments (12) freestar.

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