" degenerative joint disease "
Tuesday, November 24, 2009
Brazilian Wax Then Tanning Bed?
Introduction: The EAD is perhaps one of the most common difficulties facing a SPC in his sporting life. It was formerly called "arthritis" or "Osteoarthritis" depends on the duration of the same, the degree of involvement, etc. We will make a summary of this special emphasis on what we can do to help our horse.
The beginning of this may have different origins, the most common are the traumatic (incorrect aplomb, track defects, fatigue, bump) can also be idiopathic (of unknown origin and may start as traumatic and progressing this way they are with great outpouring or quantity of liquid, which not give up and no radiographic changes), secondary to other causes (intra-articular fractures, wounds, arthritis tanks, etc), developing disease (osteochondritis, etc). What we emphasize is that any process that would trigger the inflammation in the joint can lead to EAD. Development
EAD: basically, but each day are published on the disease advances, the development and maintenance is performed by intraraticular inflammation. When an inflammatory event, arriving within the joint a large number of inflammatory cells (especially neutrophils) which overturned on the natural proteolytic enzymes, responsible for destroying even more joint tissues (synovium, cartilage, etc) and also degrade the free substances in the joint fluid , glycosaminoglycans and hyaluronic acid. This creates a pull factor for inflammatory cells, which keep the process within the joint Flogos creating a vicious cycle that hurts more and more intense the joint structures. An important detail to note about this disease is that once started, such as arthritis, osteoarthritis progresses and joint deformation, and tends to ankylosis (the union of the ends of the joint) as the final step. Once expressed this, it is worth noting that we perform on the diseased joint, it tends to slow this process, therefore we must learn to live with it. Huge efforts are being made on a scientific level in order to obtain a solution or depth of this disease in humans with mixed results, so we deduce the complexity and intricacy of this process should make every effort not to create situations conducive to the progress of EAD.
Clinical Signs: The main sign of any EAD is the joint effusion, or increased joint fluid in thereof. This was because, due to the destruction of synovial fluid components that give viscosity limit, the hyaluronic acid to compensate for too much liquid is formed, which begins to fill the fornices of the corresponding joints. This is what we call bladders. Also remember that the blood vessels have no cartilage is nourished by synovial fluid, which is of poor quality in distance education and training also makes too much of it to meet the same requirements.
Another clinical sign is also visible although sometimes less so, is claudication, which depends on the joint and the degree of involvement.
A component to consider is the synovial fluid. Here is what the vet can see the color, this is normally yellow amber, and in increasing the tone it will turn orange, which marks the dead red blood cells due to increased training and more intense in large lesions, in cases of intra-articular fractures leaves the blood-stained fluid, because cartilage has no blood vessels and blood travels through the bone lesion. It also takes into account the viscosity of joint fluid. This is determined by the presence of hyaluronic acid, which makes lubricant, but increased the disease, enzymes and destroy this component gets more fluid. You can also evaluate the quality of hyaluronic acid Muscina test, the presence of cells, and glucose if we consider the presence of an infection inside the joint.
For the next note, treatment options, modification of training.
Galen.
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