list types f clotting mechanisms add a note on anticoagulants and hemophilia
Answers
Vascular Spasm:
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.
Platelet Plug Formation:
When blood platelets encounter a damaged blood vessel they form a “platelet plug” to help to close the gap in the broken blood vessel. (The key stages of this process are called platelet adhesion, platelet release reaction, and platelet aggregation)
Coagulation:
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. This is the beginning of the process of the blood “breaking down” from its usual liquid form in such a way that its constituents play their own parts in processes to minimize blood loss.
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). Blood clotting (technically “blood coagulation”) is the process by which (liquid) blood is transformed into a solid state.
This blood clotting is a complex process involving many clotting factors (incl. calcium ions, enzymes, platelets, damaged tissues) activating each other.
Anticoagulants:
Anticoagulants are medicines that prevent the blood from clotting as quickly or as effectively as normal.
Anticoagulants are used to treat and prevent blood clots that may occur in your blood vessels. Blood clots can block blood vessels (an artery or a vein). A blocked artery stops blood and oxygen from getting to a part of your body. Anticoagulants are used to prevent blood clots as well - the most common condition for this is atrial fibrillation (AF).
Haemophilia:
This disorder is characterized by uncontrolled bleeding and inability of the blood to clot properly. Even a small cut or a minor injury can result in severe bleeding. Haemophilia is one among the many X-linked recessive inherited genetic disorders.It results in massive internal bleeding (known as haemorrhaging) in the joints such as the knees, elbows, ankles, and also in the tissues and muscles. This can lead to considerable consequences, such as swelling and pain in the affected areas. It can even cause permanent damage to the affected body parts. When bleeding happens in a vital organ, especially in the brain, it has the potential to turn fatal.
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Answer:
Introduction
Blood is a necessary component of the human body, and the loss of this fluid may be life-threatening. Blood is generated via hematopoiesis and ultimately becomes the delivery method for oxygen to the tissues and cells. The human body protects against loss of blood through the clotting mechanism. Vascular mechanisms, platelets, coagulation factors, prostaglandins, enzymes, and proteins are the contributors to the clotting mechanism which act together to form clots and stop a loss of blood. 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.
Cellular
The cellular components of the clotting mechanism include platelets, endothelial cells, and a series of proteins, enzymes, and ions.
Organ Systems Involved
The clotting mechanism involves the circulatory system which includes the lineage of blood cells and blood vessels.
Mechanism
The clotting mechanism is broken into 2 stages.
Primary hemostasis: Formation of a weak platelet plug
Secondary hemostasis: Stabilizing the weak platelet plug into a clot by the fibrin network
Primary Hemostasis
Primary hemostasis is the formation of a weak platelet plug which is achieved in four phases: vasoconstriction, platelet adhesion, platelet activation, and platelet aggregation.
Vasoconstriction is the initial response whenever there is vessel injury. 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 (vWF), releases ATP, and inflammatory mediators. vWF is synthesized by megakaryocytes which later gets stored in a-granules of platelets. Weibel-Palade bodies of the endothelium also synthesize vWF. 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.
Secondary Hemostasis
Secondary hemostasis involves the clotting factors acting in a cascade to ultimately stabilize the weak platelet plug. This is accomplished by completing three tasks: (1) triggering activation of clotting factors, (2) conversion of prothrombin to thrombin, and (3) conversion of fibrinogen to fibrin. These tasks are accomplished initially by 1 of 2 pathways; the extrinsic and intrinsic pathway, which converge at the activation of factor X and then complete their tasks via the common pathway. Please note that calcium ions are required for the entire process of secondary hemostasis.
The extrinsic pathway includes tissue factor (TF) and factor VII (FVII). It is initiated when TF binds to FVII, activating FVII to factor VIIa (FVIIa), forming a TF-FVIIa complex. This complex, in turn, activates factor X (FX). Note, the TF-FVIIa complex can also activate factor IX of the intrinsic pathway, which is called the alternate pathway. Once Factor X is activated to FXa by TF-FVIIa complex, the cascade continues down the common pathway.
Pathophysiology
Thrombosis is the process of blood clot (thrombus) formation in a blood vessel. Virchow triad is an important concept that highlights the primary abnormalities in pathology that can lead to the clotting mechanism proceeding to thrombosis. The triad is composed of stasis or turbulent blood flow, endothelial injury, and hypercoagulability of the blood.
Abnormal (stasis) or turbulent blood flow can lead to thrombosis. Normal blood flow is laminar. Turbulent blood flow leads to endothelial injury thus promoting the formation of a thrombus. An example of turbulent blood flow is in the aneurysm of weakened vessels. Another aspect of abnormal blood flow, venous stasis, such as in post-operative bed rest, long distance traveling in a car or plane, or immobility due to obesity can lead to endothelial injury thus promoting thrombosis.
Platelet dysfunction, or clotting factor dysfunction, can be further broken down into which part of the clotting mechanism physiology is affected.
Disorders of Primary Hemostasis: vWF, Platelet defects, or Receptor Interference
Von Willebrand Factor disease
Bernard-Soulier disease
Glanzmann thrombasthenia
Medication-induced
Disorders of Secondary Hemostasis: Clotting Factor Defects