3 mechanisms that contribute to hemostasis and blood clotting

The fibrinolytic system

-dissolves small, inappropriate clots; it also dissolves clots at a site of damage once the damage is repaired.

Hemostasis

-a sequence of responses that stops bleeding. -When successful, hemostasis prevents hemorrhage.

serum

-The straw‐colored liquid after the gel separates from liquid. -blood plasma minus the clotting proteins.

hemorrhage

-Bleeding; the escape of blood from blood vessels, especially when the loss is profuse. -Hemostatic mechanisms can prevent hemorrhage from smaller blood vessels, but extensive hemorrhage from larger vessels usually requires medical intervention.

vascular spasm

-Contraction of the smooth muscle in the wall of a damaged blood vessel to prevent blood loss. -reduces blood loss for several minutes to several hours. -The spasm is probably caused by damage to the smooth muscle, by substances released from activated platelets, and by reflexes initiated by pain receptors.

platelet plug

-The first step in formation of a clot; fragile plug that slows blood flow in small wounds. -A platelet plug can stop blood loss completely if the hole in a blood vessel is small enough

thrombosis

-The formation of a clot in an unbroken blood vessel, usually a vein. -If blood clots too easily, the result can be thrombosis.

The Common Pathway for clotting

-The formation of prothrombinase is the beginning of the common pathway. -in the 2nd stage of blood clotting, prothrombinase and calcium catalyze the conversion of prothrombin to thrombin. -In the 3rd stage, thrombin, in the presence of calcium, converts fibrinogen, which is soluble, to loose fibrin threads, which are insoluble. -Thrombin also activates factor XIII (fibrin stabilizing factor), which strengthens and stabilizes the fibrin threads into a sturdy clot. -Plasma contains some factor XIII, which is also released by platelets trapped in the clot. -Thrombin has two positive feedback effects. In the first positive feedback loop, which involves factor V, it accelerates the formation of prothrombinase. -Prothrombinase in turn accelerates the production of more thrombin, and so on. -In the second positive feedback loop, thrombin activates platelets, which reinforces their aggregation and the release of platelet phospholipids.

clot

-The gel. -consists of a network of insoluble protein fibers called fibrin in which the formed elements of blood are trapped.

clotting or coagulation

-The process of gel formation. -a series of chemical reactions that culminates in formation of fibrin threads. -complex cascade of enzymatic reactions in which each clotting factor activates many molecules of the next one in a fixed sequence. -Finally, a large quantity of product (the insoluble protein fibrin) is formed.

steps of platelet plug formation: 3. platelet aggregation:

-The release of ADP makes other platelets in the area sticky, and the stickiness of the newly recruited and activated platelets causes them to adhere to the originally activated platelets. -Eventually, the accumulation and attachment of large numbers of platelets form a mass called a platelet plug.

platelet derived growth factor (PDGF)

-a hormone that can cause proliferation of vascular endothelial cells, vascular smooth muscle fibers, and fibroblasts to help repair damaged blood vessel walls.

steps of platelet plug formation: 2. platelet release reaction:

-adhesion activates platelets, and characteristics change. grow projections that enable them to interact with one another. -they begin to liberate the contents of their vesicles. -Liberated ADP and thromboxane A2 play a major role by activating nearby platelets. -Serotonin and thromboxane A2 function as vasoconstrictors, causing and sustaining contraction of vascular smooth muscle, which decreases blood flow through the injured vessel.

plasminogen

-an inactive plasma enzyme that is incorporated when a clot is formed. -can be activated and transformed from plasminogen to plasmin. -it becomes activated by substances in blood and body tissues. these substances include: thrombin, activated factor XII, and tissue plasminogen activator (t‐PA),

Intravascular Clotting

-blood clots that form within the cardiovascular system. -initiated by roughened endothelial surfaces of a blood vessel resulting from atherosclerosis, trauma, or infection. -These conditions induce adhesion of platelets. -may also form when blood flows too slowly (stasis), allowing clotting factors to accumulate locally in high enough concentrations to initiate coagulation

Blood Clotting

-blood remains in its liquid form as long as it stays within its vessels. -If it is drawn from the body, however, it thickens and forms a gel. -Eventually, the gel separates from the liquid.

clotting (coagulation) factors.

-calcium ions. -several inactive enzymes that are synthesized by hepatocytes (liver cells) and released into the bloodstream. -various molecules associated with platelets or released by damaged tissues. -identified by Roman numerals that indicate the order of their discovery.

steps of platelet plug formation: 1. platelet adhesion:

-contact and stick to parts of a damaged blood vessel, such as collagen fibers of the connective tissue underlying the damaged endothelial cells.

The extrinsic pathway of blood clotting

-fewer steps than the intrinsic pathway and occurs rapidly—within a matter of seconds. -tissue factor (TF), also known as thromboplastin, leaks into the blood from cells outside (extrinsic to) blood vessels and initiates the formation of prothrombinase. -TF is a complex ixture of lipoproteins and phospholipids released from the surfaces of damaged cells. -In the presence of calcium, TF begins a sequence of reactions that ultimately activates clotting factor X. -Once factor X is activated, it combines with factor V in the presence of to form the active enzyme prothrombinase, completing the extrinsic pathway.

The intrinsic pathway of blood clotting

-more complex and it occurs more slowly, usually requiring several minutes. -its activators are either in direct contact with blood or contained within (intrinsic to) the blood; outside tissue damage is not needed. -If endothelial cells become roughened or damaged, blood can come in contact with collagen fibers in the connective tissue around the endothelium of the blood vessel. -trauma to endothelial cells causes damage to platelets, resulting in the release of phospholipids by the platelets. -Contact with collagen fibers (or with the glass sides of a blood collection tube) activates clotting factor XII, which begins a sequence of reactions that eventually activates clotting factor X. -Platelet phospholipids and calcium can also participate in the activation of factor X. -Once factor X is activated, it combines with factor V to form the active enzyme prothrombinase.

Platelet Plug Formation

-platelets store a lot of chemicals in vesicles. -these chemicals are good for blood clotting. (ADP, ATP, Calcium, serotonin) -also contain enzymes that produce thromboxanne strengthen blood clots. -also within platelets is platelet derived growth factor.

anticoagulants

-substances that delay, suppress, or prevent blood clotting. -present in blood.

Clot Retraction

-the consolidation or tightening of the fibrin clot. -The fibrin threads attached to the damaged surfaces of the blood vessel gradually contract as platelets pull on them. -depends on an adequate number of platelets in the clot, which release factor XIII and other factors, thereby strengthening and stabilizing the clot. -As the clot retracts, it pulls the edges of the damaged vessel closer together, decreasing the risk of further damage. -During retraction, some serum can escape between the fibrin threads, but the formed elements in blood cannot. -Normal retraction Permanent repair of the blood vessel can then take place. In time, fibroblasts form connective tissue in the ruptured area, and new endothelial cells repair the vessel lining.

Role of Vitamin K in Clotting

-vitamin K is not involved in actual clot formation. -is required for the synthesis of four clotting factors. -produced by bacteria that inhabit the large intestine. -fat‐soluble vitamin that can be absorbed through the lining of the intestine and into the blood if absorption of lipids is normal.

Clotting can be divided into three stages:

1. -Two pathways, called the extrinsic pathway and the intrinsic pathway, lead to the formation of prothrombinase. -Once prothrombinase is formed, the steps involved in the next two stages of clotting are the same for both the extrinsic and intrinsic pathways, and together these two stages are referred to as the common pathway. 2. -Prothrombinase converts prothrombin (a plasma protein formed by the liver) into the enzyme thrombin. 3. -Thrombin converts soluble fibrinogen (another plasma protein formed by the liver) into insoluble fibrin. Fibrin forms the threads of the clot.

Three mechanisms reduce blood loss:

1. vascular spasm, 2. platelet plug formation, 3. blood clotting (coagulation).

review

A blood clot is a gel that contains formed elements of the blood entangled in fibrin threads.

embolus

A blood clot, bubble of air or fat from broken bones, mass of bacteria, or other debris or foreign material transported by the blood.

thrombus

A stationary clot formed in an unbroken blood vessel, usually a vein.

Along with platelet plug formation, which two mechanisms contribute to hemostasis?

Along with platelet plug formation, vascular spasm and blood clotting contribute to hemostasis.

activated protein C (APC)

An anticoagulant that inactivates the two major clotting factors not blocked by antithrombin and enhances activity of plasminogen activators. -Babies that lack the ability to produce APC due to a genetic mutation usually die of blood clots in infancy.

thrombosis

Clotting in an unbroken blood vessel (usually a vein)

fibrinolysis

Dissolution of a clot is called

review

In blood clotting, coagulation factors are activated in sequence, resulting in a cascade of reactions that includes positive feedback cycles.

plasmin

Once plasmin is formed from plasminogen, it can dissolve the clot by digesting fibrin threads and inactivating substances such as fibrinogen, prothrombin, and factors V and XII.

pulmonary embolism.

a condition when an embolus lodges in the lungs

antithrombin:

an anticoagulant that blocks the action of several factors, including XII, X, and II (prothrombin).

Heparin

an anticoagulant that is produced by mast cells and basophils, combines with antithrombin and increases its effectiveness in blocking thrombin.