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Sock's Toxicity And Drugs In RA:
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Patients with autoimmune diseases have antibodies in their blood which target their own tissues which can be associated with inflammation. There is no known cure for RA or means of preventing it. Optimal management requires early diagnosis and timely introduction of agents that reduce the probability of irreversible joint damage.
 
Periodic assessment of disease activity,drug toxicity,and the effectiveness of the treatment program is essential,with revisions of the treatment program as necessary.
 
Rheumatoid arthritis does not affect everyone in the same way,some will have the mild form,and others will have the moderate or severe form. Treatment and disease duration is also variable according to individual patient.
 
Early RA (less than 2 years )is the best time for treatment.The majority of patients have intermittent or steady progression of the disease and require continued treatment (progressive). If  and when  the symptoms of disease have subsided or have been successfully treated it is called remission.
 
Historically RA was classified in terms of how it interfeared with normal  everyday functioning:
 
1) Normal function.
 
2) Mildly limited function.
 
3) Moderately limited function.
 
4) Severely limited function (disabled).
 
And by bone damage caused by the disease that shows up on a x-ray film:
 
1) Normal bone.
 
2) Some bone change.
 
3) Moderate bone change.
 
4) Extensive bone change.
 
This classification shows how much damage the inflammation associated with RA has already done,but it does not help to show how severe or how fast the RA will progress.
 
The course of RA could be better classified by:
 
Mild,Moderate and Severe-and by how long it has been present.
 
1) Early (less than 2 years) -the best time for treatment.
 
2) Progressive-the majority of patients at this stage have intermittent or steady progression of the disease and need continuing treatment.
 
3) Controlled-when the symptoms of disease is in remission.
 
The inflammation asociated with RA also occurs outside the joints. Since RA can cause extra-articular features (described on my other site),it can be viewed as a disease  that can affect the whole body not just the joints.
 
EAFs can affect how you function,how you feel, and the quality of your life. EAFs affect the tendons,heart,lungs,nervous system, blood vessels,eyes and rheumatoid nodules may appear underneath the skin. EAFs are more common in the moderate and severe types of RA. They are usually  absent in the mild type of RA.
 
Many patients with the more severe type of RA feel ill as if they have a chronic bad flu. Patients feel tired,have no energy,feel nauseated,lose their appetite,and sometimes even lose weight. These symptoms are typical of RA and are called constitutional features.
 
All patients with RA feel unwell but patients with moderate and severe feel unwell the most. Like extra-articular features,the severity of these symptoms helps to separate RA from other forms of arthritis.
 
When determining the type of RA we must consider the following:
 
The severity:
 
1) Is the arthritis mild,moderate,or severe? Is it characterized more by "stiffening" than by swelling?
 
2) The rheumatoid factor test: The level of RF,an antibody found in the blood has known effects in the immune system,is partially related to the severity of RA. Patients with moderate or severe disease usually have much higher levels of RF than people with mild arthritis. Up to 20% of RA patients however never develop R.F.
 
10 to 15% of all RA patients have the type of arthritis characterized by stiffness. This type of RA leads to abnormal tightness rather than to swelling in the small joints of the hands,wrists,shoulders, and some patients have problems with the knees and feet. The stiffness is profoundly marked.  
 
Although the joints may look normal,the patient may find it very difficult to hold a glass of water or to lift their arms over their head. Normal every day activities can become impossible within a matter of weeks with this form of disease.
 
With the exception of inflammation of the tendons (tendonitis),E.A.F.'s are rare in this type of RA. The R.F. and the test for HLA genes are usually negative.Loss of function is the major problem caused by this stiffness. One may find it very difficult to move and do things normally, and if left untreated this loss can be pronounced and irreversible.
 
HLA genes were always associated with severity,but some recent research suggests,it may be less important. The debate continues.
 
In most patients,the type of RA  diagnosed at onset persists during the entire course of their disease. However,in some patients,the type do change. This usually happens early in the disease,before the full features of either moderate or severe RA have developed, making them difficult to distinguish from the mild form of disease.
 
Unfortunety, the disease most often "comes in quite and goes out with a roar". The opposite is rarely true. It is uncommon for moderate or severe disease to become mild without treatment.
 
Permanent deformity is a unwanted result of the inflammatory process. Persistent tenosynovitis and synovitis leads to the formation of synovial cysts and to displaced or ruptured tendons. Extensor tendon rupture at the dorsum of the hand is a common and disabling problem.
 
Bony erosions seen at the margins of the joint,at the attatchment of the synovium,are the hallmark of RA. Erosions occur rapidly within the first 2 years of the disease. These anatomic changes result in limitations in range of motion,flexion contractures,and subluxation (incomplete dislocation) of articulating bones.
 
A mild anemia with hematocrit values in the range of 30-34% occurs in approximately 25 to 35% of patients with RA. In most cases, the reduced red cell mass is caused by the anemia of chronic disease,a normocytic-normochromic process charachterized by a low concentration of serum iron,a low serum iron-binding capacity,and a normal or increased serum ferritin concentration.
 
However, occasionally  true iron deficiency anemia can develop secondary to intercurrent blood loss often from gastrointestinal (GI) bleeding due to NSAIDs.

Finding a balance between rest and exercise is crucial to managing the disease. In order to strike the right balance,it is essential that the patient learn to listen to their body. when the symptoms flare--when the joints are sore,warm,and swollen--take it easy,make time to rest. At these times,continue to perform range-of-motion exercise to keep the body mobile,but be careful not to tire yourself or aggravate the joints.
 
Avoid unnecessary walking,housework or other activities. When the joints feel better and when other symptoms,including fatigue and morning stiffness,are less noticeable,increase the activity level.
 
Moderate weight-bearing exercises,such as walking and lifting light weights,can strengthen weakened muscles without risking additional joint damage. If exercise produces more pain or joint swelling--cut back a bit or stop the exercise that causes pain. Exercise should not be painful.
 
Conclusion of the consensus panel on optimal calcium intake-- On the basis of the most current information available,optimal calcium intake is estimated to be Recommended daily intake for men is 1000mg/day (25-65 years). For all men and women over 65,daily intake is recommended to be 1,500mg/day.although further research in this age group.
 
These guidlines are based upon calcium from the diet plus any calciium taken in supplementary form. Adequate vitamin D is essential for calcium absorption. Dietary constituents,drugs,age, and genetic factors influences the amount of calcium required for optimal skeletal health. Calcium intake,up to a total intake of 2000mg/day appears to be safe in most individuals.
 
The preferred source of calcium is through calcium rich-foods as diary products. Calcium-fortified foods and calcium supplements are other means by which optimal calcium intake can be reached in those who cannot meet the ned by ingesting conventional foods.
 
The course of rheumatoid arthritis cannot be predicted in a given patient. Several patterns of activity have been described:
 
*A spontaneous remission particularly in the seronegative patient within the first 6 months of symptoms (less than 10%).
 
* Recurrent explosive attacks followed by periods of quiescence most commonly in the early phases.
 
*The usual pattern of persistent and progressive disease activity that waxes and wanes in intensity.
 
* Disability is higher among patients with rheumatoid arthritis with 60% being unable to work 10 years after the onset of their disease.
 
* Recent studies have demonstrated an increased mortality in RA patients. Median life expectancy was shortened an average of  7 years for men and 3 years for women compared to controlled populations.
 
In more than 5000 patients with RA from 4 centres,the mortality rate was two times greater than in the control population. Patients at higher risk for shortened survival are those with systemic extra-articular involvement,low functional capacity,low social economic status,low education,and prednisone use.(what has low education got to do with it ? )

AOL RA Links

Rheumatoid Arthritis Basics:

My Personal Experience with RA:

Factors Involved In The Disease Process:
 
Rheumatoid Arthritis can attack any synovial joint in the body. Early in the course of the disease several changes in joint structures occur. Joint effusion and inflammation of the synovium occur,producing a soft tissue swelling that is easily detected during evaluation of the patient. Additionally,changes (osteoporosis) in the ends of the bones may be present early in the disease process.
 
A synovial joint has the following components:
 
1) A joint capsule that isolates the joint from surrounding tissue.
 
2) A joint cavity formed by the surrounding joint capsule.
 
3) A synovial membrane (synovium) that is the inner linning of the joint capsule
 
4) Synovial fluid that is secreated by the synovium and serves as a lubricant and carries nutrients for the joint.
 
5) Bones that come together to form the joint.
 
6) Hyaline (articular) cartilage covers and protects the ends of the bones that participate in the joint.
 
There will be other structures present or near the joint such as disks,cartilage (menisci),tendons,and ligaments.
 
Important characteristics Of these structures to remember are:
 
1) The joint capsule is composed of two layers,an outer fibrous layer and the inner synovium. The outer layer has many joint receptors innervating it,but is not well vascularized. The opposite is true with the synovium. i.e.,it is well vascularized but poorily innervated.
 
2) The articular cartilage has two important functions including the ability to minimize friction and wear between two opposing joint surfaces during movement and to dissipate forces on the joint over a wider area,thus decreasing stresses on the contacting joint surfaces.
 
3)Synovial fluid contains hyaluronate (hyaluronic acid) and a glycoprotein called lubricin. Both are responsible for the lubrication of the joint,although they are specific for certain components. Hyaluronic acid is important for the lubrication of the joint capsule while lubricin is necessary for cartilage on cartilage lubrication.
 
4)Synovial fluid is also the median by which nutrients are carried to,and wastes are carried from,the avascular components of the joint.
 
5)The ends of the long bones that form the synovial joints are composed of a soft,spongy type of bone called subchondral bone.
 
Hyaline (articular) cartilage covers this bone and protects it. Except for the very ends of the bone,long bones are usually very strong.
 
The attack on a joint by the disease usually occurs begins with the synovium. Early in the disease,edema begins to be seen in the cells in the synovium and mutiplication of synovial lining cells occur.
 
As the disease progresses,the synovium may grow considerably larger,(thicker) eventually forming tissue called pannus. Pannus can be considered the most destructive element affecting joints in the patients with RA. Pannus can attack articular cartilage and destroy it. Further,pannus can destroy the soft subcondral bone once the protective articular cartilage is gone.
 
The synovial fluid secreted by the synovium is thought to serve two main purposes,lubrication of the joint,and provision of nutrients to the avascular articular cartilage. In this disease process,an interaction between antibodies and antigens occurs,and causes alterations in the composition of the synovial fluid.
 
Ultimately,digestants are (such as cytokines) formed in the fluid which attack the surrounding tissue. Once the composition of this fluid is altered, it is less able to perform the normal functions,and more likely to become destructive.
 
The changes in the synovium and synovial fluid are responsible for a large amount of joint and soft tissue destruction. The destruction of bone eventually leads to laxity in tendons and ligaments.
 
Under the strain of daily activities and other forces,these alterations in bone and joint structure result in the deformities   frequently seen in patients with RA. Considerable destruction of the joint can occur with pannus invading the subchondral bone.
 
Bone destruction occurs at areas where the hyaline cartilage and the synovial lining do not adequately cover the bone.
 
If the disease progresses to a more advanced stage,the articular cartilage may lose its structure and density resulting in an inability to withstand the normal forces placed on the joint. In these advanced cases,muscle activity causes the the involved ends of the bones to be compressed together causing further bone destruction.
 
Further,the disease  can irreversibily change the structure and function of a joint to a degree that other degenerative changes may occur,especially in the weight bearing joints of the body. Thus,joint destruction can progress to the degree that joint motion is significantly limited and joints can become markedly unstable.
 
Inflammation in RA is a very complex process. We velieve it starts when one one of the class of cells that guards the body against foreign invaders ( in ordinary inflammation these are usually bacteria or viruses) comes into contact with something that triggers the alarm. One form the alarm takes is a whole battery of chemical messengers,called cytokines,that are released into the joint.
 
 These recruit other cells,the white blood cells that attack and kills other cells and vacteria. One form this killing takes is the release into the immediate area of very "corrosive"" chemicals. Joint tissue,an innocent bystander,is damaged.
 
 Furthermore,cytokines stimulate the lining of the joint (synovial lining ) to grow and produce other chemicals that break down cartilage. Cytokines are released into the blood stream,and cause fever and fatigue. The body is so finely balanced,there are also cytokines released that tend to damp down the inflammation.
 
Unfortunately,in the RA joint these "good" cytokines tend to become overwhelmed by the "bad" or pro-inflammatory cytokines. One of the key cytokines that promote inflammation is TNF-alpha. IL-1  alpha is another-there are many members of the IL.group.
 
Glucocorticoid use is the most common form of drug-related osteoporosis,and its long term administeration for disorders such as RA.Osteoporosis is defined as a skeletal disorder charachterized by comprimisal bone strength predisposing  to an increased risk of fracture. Bone strength reflects the integration of two more of the criterias.
 
Bone density is expressed as grams per area or volume in any given individual is determined by peak bone mass and amount of bone loss.Bone quality refers to architecture,turnover,damage accumulation (e.g., microfractures) and minerilization.
 
It is important to acknowledge a common misperception is that osteoporosis is always the result of bone loss. Bone loss commonly as one ages,but an individual who does not reach optimal (i.e. peak) bone mass during childhood, and adolescense may develop osteoporosis  without the occurrance of accellerated bone loss.
 
Hence sub optimal bone growth in childhood and adolescence is an important as bone loss to the development of osteoporosis.