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Von Willebrand'S Disease In Dogs

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Abstract

Von Willebrand's Disease is a genetic coagulation disorder that specifically affects the production of the von Willebrand Factor protein. This protein is a vital component for primary Hemostasis and the Coagulation process. Without von Willebrand Factor, or abnormal levels of it, production of other vital proteins will be impeded thus causing the whole process to fail or slow down. The canis domesticus species (dogs) is the animal model of focus for this report. Through studying other animal models, we can become more familiar with the disease as well as note any common links. This will aid in prevention, treatment, and ultimately curing the disease.

Introduction

Erik von Willebrand first described human von Willebrand's disease (vWd) in 1926. About four and a half decades later, in 1970, the first case of canine von Willebrand's disease was described. This first case was seen in the German Shepherd breed. Today many cases of von Willebrand's disease occurs in more than 50 breeds of dog. vWd is an autosomal genetic bleeding disorder and is known to be the most common bleeding disorder in humans, dogs, and many other animal species.1

Today one possible definition of life, according to our course manual is,

"The state of physical entities that utilize substances and energy from outside themselves for the purposes of growth, the repair of their own structure, the maintenance of their functional systems, and that are capable of self-replication."2

The ability to 'repair' one's self is what von Willebrand's disease is most concerned with. Specifically, it is the ability to form blood clots.

Blood Clotting

The clotting process is a complex and vital mechanism in protecting the body from illness and/or death. Thus, in order to better understand what von Willebrand's disease is, what it does, and its affects, we first must have a basic understanding of blood and what occurs normally within the damaged vessels.

Normally, bleeding is stopped by the formation of a platelet plug and a blood clot, this is called homeostasis and is very important for survival. Following the loss of vascular integrity the main steps of homeostasis are, in order:

1. Vascular constriction. This limits the flow of blood to the area of injury.

2. Platelets become activated by thrombin and aggregate at the site of injury forming a temporary, loose platelet plug.

3. Insuring stability of the initially loose platelet plug, a fibrin mesh (the blood clot) forms and entraps platelets and red blood cells.

Now, a closer look at these main steps of homeostasis:

1. Immediately the damaged vessel or capillary constricts to lessen the blood loss. This is called vasoconstriction. Also, the damaged cells release chemicals that aid in the whole process and cause substances to get sticky.

2. Platelets adhere to the collagen that is exposed from the damaged area and form a temporary plug.

When the platelets bind to the collagen, they activate or 'turn on'. When activated, degranulation occurs, the process which releases serotonin, ADP, and Thromboxane A2 from the platelets. Serotonin is a vasoconstrictor, ADP (adenosine di-phosphate) attracts more platelets to the area, and Thromboxane A2 encourages platelets aggregation, degranulation, and vasoconstriction.

Next is one of the most important and complicated parts of step 2, coagulation. There are many subsets, including many factor proteins, that all depend on each other in order to successfully work. There are two initial pathways, the intrinsic and extrinsic pathways. The extrinsic pathway starts with the protein TF (tissue factor, also referred to as Factor III or thromboplastin) being released from the surface of the damaged cells. TF, with the help of Ca2+ ions, come together to activate Factor VII. This TF-VII heterodimer is a protease, with Factor X and Factor IX as substrates.

The initiation of the intrinsic pathway is caused by Factor XII, from the active platelets. This pathway uses Factor IX which permits Factor VIII (a protein that readily circulates in the blood) to bind to it. Von Willebrand's Factor (vWF) protein binds to Factor VIII. This is where Hemophilia A and von Willibrand's disease are easily misdiagnosed. A decreased Factor VIII causes Hemophilia A however, decreased amounts of vWF is the cause for von Willebrand's disease. Factor XI assists in the production of Factor IX. All of these Factors working together initiate the activation of Factor X.

As we can see, the products of both pathways are Factor X, however both pathways together are needed to promote the cascade reactions that activate Factor X. Once Factor X is activated, added with Factor III, Factor V, Ca2+ and PF3 (platelet thromboplastic factor), Prothrombin activator becomes activated. This converts prothrombin (Factor II) to thrombin. The thrombin converts fibrinogen (Factor I) to fibrin then the fibrin forms a loose mesh of fibrinopeptides. Thrombin also activates Factor XIII (a fibrin stabilizer) which forms covalent cross links that convert the loose mesh to a dense aggregation of fibers.

3. Lastly, red blood cells and platelets get caught in the dense mesh causing a completed protective wall. This entails the formation of a blood clot.

Now, that the general formation of a blood clot is known, a better understanding of what is going on in von Willebrand's disease will follow.

Von

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