Intrinsic and extrinsic coagulation pathways pdf

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intrinsic and extrinsic coagulation pathways pdf

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The article also illustrates the appropriateness of monitoring treatment in specialist units to maintain the level of anticoagulation within the very narrow margin that allows prevention of thrombosis without causing bleeding complications.

All the components necessary for the clotting process to proceed are found in the blood. As such, the proteins required for such clotting to take place are part of the intrinsic pathway of blood coagulation. This pathway involves a series of proteins, protein cofactors, and enzymes, which interact in reactions that take place on membrane surfaces. These reactions are initiated by tissue injury and result in the formation of a fibrin clot Figure 1. The intrinsic pathway is initiated by the activation of factor XII by certain negatively charged surfaces, including glass.

16.5D: Coagulation

Coagulation is the process by which a blood clot forms to reduce blood loss after damage to a blood vessel. Several components of the coagulation cascade, including both cellular e. The role of the cellular and protein components can be categorized as primary hemostasis the platelet plug and secondary hemostasis the coagulation cascade. The coagulation cascade is classically divided into three pathways: the contact also known as the intrinsic pathway, the tissue factor also known as the extrinsic pathway , and the common pathway.

Both the contact pathway and the tissue factor feed into and activate the common pathway. Hemostasis can either be primary or secondary. Primary hemostasis refers to platelet plug formation, which forms the primary clot. Secondary hemostasis refers to the coagulation cascade, which produces a fibrin mesh to strengthen the platelet plug.

Secondary hemostasis occurs simultaneously with primary hemostasis, but generally finishes after it. The coagulation factors circulate as inactive enzyme precursors, which, upon activation, take part in the series of reactions that make up the coagulation cascade. The coagulation factors are generally serine proteases enzymes.

The intrinsic pathway contact activation pathway occurs during exposure to negatively charged molecules, such as molecules on bacteria and various types of lipids. The extrinsic pathway occurs during tissue damage when damaged cells release tissue factor III.

Tissue factor III acts on tissue factor VII in circulation and feeds into the final step of the common pathway, in which factor X causes thrombin to be created from prothrombin.

In the final common pathway, prothrombin is converted to thrombin. When factor X is activated by either the intrinsic or extrinsic pathways, it activates prothrombin also called factor II and converts it into thrombin using factor V. Thrombin then cleaves fibrinogen into fibrin, which forms the mesh that binds to and strengthens the platelet plug, finishing coagulation and thus hemostasis.

It also activates more factor V, which later acts as an anticoagulant with inhibitor protein C, and factor XIII, which covalently bonds to fibrin to strengthen its attachment to the platelets. While the coagulation cascade is critical for hemostasis and wound healing, it can also cause problems. An embolism is any thrombosis blood clot that breaks off without being dissolved and travels through the bloodstream to another site.

If it obstructs an artery that supplies blood to a tissue or organ, it can cause ischemia and infarcation to those tissues, leading to a pulmonary embolism, stroke, or heart attack. Coagulation can occur even without injury, as blood pooling from prolonged immobility can cause clotting factors to accumulate and activate a coagulation cascade independently. Additionally, endothelial damage caused by immune system factors like inflammation or hypersensitivity may also cause unnecessary thrombosis and embolism.

For example, during severe bacterial infections septic shock , inflammation-induced tissue damage and the negatively charged molecules of bacteria activate both pathways of the coagulation cascade and cause disseminated intravascular coagulation DIC , in which many clots form and break off, leading to massive organ failure. Many anticoagulants prevent unnecessary coagulation, and those that genetically lack the ability to produce these molecules will be more susceptible to coagulation.

These mechanisms include:. Learning Objectives Outline the process of coagulation in secondary hemostasis. Key Points The coagulation cascade is a series of reactions, which is classically divided into three pathways: the contact also known as the intrinsic pathway, the tissue factor also known as the extrinsic pathway , and the common pathway.

The intrinsic pathway occurs when negatively charged molecule contact causes a cascade of factors that produce factor X. The extrinsic pathway occurs when tissue damage causes the release of tissue factor, creating a smaller cascade that produces factor X. The common pathway merges both pathways as factor X is used to create thrombin from prothrombin.

Secondary hemostasis involves factors of the coagulation cascade, which collectively strengthen the platelet plug. Coagulation can be harmful if blood clots embolize and obstruct other blood vessels.

Clots can also occur if blood pools from prolonged immobility. A number of anticoagulants exist to inhibit various parts of the coagulation cascade, inactivate thrombin, or degrade fibrin directly. Key Terms fibrin : An elastic, insoluble, whitish protein produced by the action of thrombin on fibrinogen and forming an interlacing fibrous network in the coagulation of blood. Coagulation Pathway. Secondary Hemostasis Hemostasis can either be primary or secondary.

Coagulation Cascade. Intrinsic Pathway The intrinsic pathway contact activation pathway occurs during exposure to negatively charged molecules, such as molecules on bacteria and various types of lipids. Common Pathway In the final common pathway, prothrombin is converted to thrombin. Coagulation Problems While the coagulation cascade is critical for hemostasis and wound healing, it can also cause problems. Anticoagulants Many anticoagulants prevent unnecessary coagulation, and those that genetically lack the ability to produce these molecules will be more susceptible to coagulation.

Plasmin: generated by proteolytic cleavage of plasminogen, a potent fibrinolytic that degrades fibrin and destroys clots. Prostacyclin PGI2 : released by the endothelium and inhibits platelet activation. Thrombomodulin: released by the endothelium and converts thrombin into an inactive form.

The extrinsic pathway of blood coagulation

Thrombin generation TG is a pivotal process in achieving hemostasis. Coagulation profiles during pregnancy and early neonatal period are different from that of normal non-pregnant adults. In this ex vivo study, the differences in TG in maternal and cord plasma relative to normal adult plasma were studied. Twenty consented pregnant women and ten consented healthy adults were included in the study. Maternal and cord blood samples were collected at the time of delivery. Platelet-poor plasma was isolated for the measurement of TG. Additionally, procoagulant and inhibitor levels were measured in maternal and cord plasma, and these values were used to mathematically simulate TG.

Blood coagulation refers to the process of forming a clot to stop bleeding. Coagulation is a complicated subject and is greatly simplified here for the student's understanding. To stop bleeding, the body relies on the interaction of three processes: Primary hemostasis involves the first two processes. Vasoconstriction is the body's first response to injury in the vascular wall. When injury occurs, vessel walls constrict, causing reduced blood flow to the site of injury.

Negreva, K. Vitlianova, R. Background: Clinical interest in the haemostasis profile of patients with paroxysmal atrial fibrillation PAF , and in particular, in blood coagulation is significant. It is known that blood coagulation is activated in two pathways: extrinsic and intrinsic. Regardless of the activation method, the coagulation cascade ends with a final common pathway, in which the activated factor X FX is central to the prothrombin complex, responsible for the conversion of prothrombin factor II F II to thrombin that converts fibrinogen into fibrin. Materials and methods: 51 non-anticoagulated patients 26 men, 25 women; mean age

A mathematical model for in vitro coagulation of blood: role of platelet count and inhibition

Upon the introduction of cells, particularly crushed or injured tissue, blood coagulation is activated and a fibrin clot is rapidly formed. The protein on the surface of cells that is responsible for the initiation of blood clotting is known as tissue factor , or tissue thromboplastin. Tissue factor is found in many of the cells of the body but is particularly abundant in those of the brain, lungs, and placenta. The pathway of blood coagulation activated by tissue factor, a protein extrinsic to blood, is known as the extrinsic pathway Figure 1.

Natalya M. Ananyeva, Diana V. Kouiavskaia, Midori Shima, Evgueni L. Saenko; Intrinsic pathway of blood coagulation contributes to thrombogenicity of atherosclerotic plaque.

Игра закончена. Червь ползет с удвоенной скоростью.

Intrinsic pathway of blood coagulation

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NDAKOTAARA. ANON. ORG Ее внимание сразу же привлекли буквы ARA - сокращенное название Анонимной рассылки Америки, хорошо известного анонимного сервера. Такие серверы весьма популярны среди пользователей Интернета, желающих скрыть свои личные данные. За небольшую плату они обеспечивают анонимность электронной почты, выступая в роли посредников.

 - Кто теперь напишет материал для моей колонки. - Сэр, я… - За все сорок три года путешествий я никогда еще не оказывался в таком положении. Вы только посмотрите на эту палату. Мою колонку перепечатывают издания по всему миру. - Сэр! - Беккер поднял обе руки, точно признавая свое поражение.

Hemostasis

Внутренний голос подсказывал Беккеру, что он что-то упустил - нечто очень важное, но он никак не мог сообразить, что. Я преподаватель, а не тайный агент, черт возьми. И тут же он понял, почему все-таки Стратмор не послал в Севилью профессионала. Беккер встал и бесцельно побрел по калле Делисиас, раздумывая на ходу, что бы предпринять. Мощенный брусчаткой тротуар под ногами постепенно сливался в одну темную гладкую полосу.

Он жестом предложил старику перешагнуть через него, но тот пришел в негодование и еле сдержался. Подавшись назад, он указал на целую очередь людей, выстроившихся в проходе. Беккер посмотрел в другую сторону и увидел, что женщина, сидевшая рядом, уже ушла и весь ряд вплоть до центрального прохода пуст. Не может быть, что служба уже закончилась. Это невозможно. Да мы только вошли. Но, увидев прислужника в конце ряда и два людских потока, движущихся по центральному проходу к алтарю, Беккер понял, что происходит.

 Да поможет нам Бог, - прошептала.  - Мы можем принять участие в аукционе. Стратмор покачал головой: - Танкадо дал нам шанс. Это совершенно ясно. Тем не менее риск велик: если нас обнаружат, это, в сущности, будет означать, что он своим алгоритмом нас напугал. Нам придется публично признать не только то, что мы имеем ТРАНСТЕКСТ, но и то, что Цифровая крепость неприступна. - Каким временем мы располагаем.

COMMENT 4

  • A mechanistic model including the role of platelets is proposed for clot formation and growth in plasma in vitro. Harnbradezpa - 22.03.2021 at 23:59
  • Secondary hemostasis includes the two main coagulation pathways, intrinsic and extrinsic, that meet up at a point to form the common pathway. Cleohuggerxp - 23.03.2021 at 22:46
  • Platelets are key players in hemostasis , the process by which the body seals a ruptured blood vessel and prevents further loss of blood. Alexandrie L. - 24.03.2021 at 16:24
  • Coagulation is the process by which a blood clot forms to reduce blood loss after damage to a blood vessel. BelГ©n S. - 26.03.2021 at 22:32

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