Rheumatoid Arthritis: Causes, symptoms, diagnosis and drug treatment

Arthritis

What is Rheumatoid Arthritis?

Rheumatoid arthritis is a chronic inflammatory rheumatic and multisystemic chronic. Generally symmetrically affects diarthrodial joints (knees, hips, hands, feet, etc.).. The progressive deterioration of the disease, articular or extraarticular, eventually leads to deformity, functional disability and reduced life expectancy.

Etiology or cause of Rheumatoid Arthritis

The etiology or cause. There are several theories, but that seems most accepted is the existence of an infectious agent on a genetically predisposed individual that would be the cause of hypertrophy and hypertrophy of synovial tissue, local or segmental vascular changes, edema (fluid accumulation) and inflammation of mononuclear cells to release a series of molecules that may be the cause of the systemic manifestations of rheumatoid arthritis (IL-1, IL-6, GM-CSF, etc.)..

Symptoms of Rheumatoid Arthritis

The predominant clinical manifestations are skeletal muscle type. Following lists the most characteristic signs or symptoms:

  • Arthritis in the joint exploration objective is swollen, hot, red and painful. Are affected symmetrically.
  • Joint stiffness: it appears after a prolonged period of inactivity. It is most noticeable in the morning and decreases with movement. If it lasts more than an hour, joint inflammation is more severe.
  • Deformities: occur by involvement of ligaments, tendons, joint capsule and cartilage over time. It is quite remarkable in their hands.
  • Rheumatoid nodules: are subcutaneous, mobile, not attached and located mainly in the extensor aspect of the forearm.
  • Caplan syndrome: is an association of neumonociosis, pulmonary rheumatoid nodules and polyarthritis (involvement of more than one joint).
  • Felty Syndrome: Rheumatoid arthritis is a chronic, associated with splenomegaly (enlarged spleen), neutropenia (decrease of granulocytes, cells that our immune system, among others), and sometimes, anemia and thrombocytopenia (decreased number of platelets in blood).

The most common manifestations are pain, joint swelling, weakness or muscle atrophy, joint stiffness, deformity, and ligamentous laxity. Usually the symptoms are usually other symptoms of general or systemic involvement.

Diagnosis of Rheumatoid Arthritis

Diagnostic tests for rheumatoid arthritis include:

  • Laboratory tests: rheumatoid factor, anti-CCP antibody (anti-CCP) and erythrocyte sedimentation rate. In addition to general analysis of blood count and basic biochemistry.
  • Aspiration: The removal of a joint synovial fluid (eg knee). Fluid are studied and inflammatory characteristics.
  • Radiology is seen rising soft spots, osteopenia (decreased bone), erosions ... Not relevant for early diagnosis. For an earlier diagnosis can be used magnetic resonance imaging and scintigraphy with Tc-99m labeled diphosphonates.

The clinical diagnosis is the absence of definitive diagnostic tests.

Drug Therapy for Rheumatoid Arthritis

The therapy is divided into a drug treatment and other non-pharmacological step.

Drug treatment step:

  • Calcium, vitamin D and bisphosphonates: to prevent or treat osteoporosis secondary to steroid treatment.
  • Analgesics and nonsteroidal antiinflammatory drugs (NSAIDs): control the symptoms and local signs of inflammation.
  • Corticosteroids: a low-dose oral inflammatory symptoms diminish rebel. There are studies that suggest the possibility of delaying the onset and progression of bone erosions. Treatment dropout patterns transitional stages.
  • Drugs Disease modifying antirheumatic drugs (DMARDs): control the progression of the disease in the long run by reducing high levels of acute phase reactants, and therefore possibly modify the inflammatory component and the destructiveness of the process. There may be associated. These are methotrexate, sulfasalazine, leflunomide, antimalarials, D-penicillamine, cyclosporine A, azathioprine, cyclophosphamide, and gold compounds. Methotrexate is usually the drug of choice, but should be administered in conjunction with folic acid and requires radiological thoracic and liver function toxicity.
  • Biological agents are directed against some components of the inflammatory response. The most commonly used are anti-TNF-α (infliximab, etarnercept, adalimumab) receptor antagonist IL-1 (anakinra), biological response modulators (abatacept and rituximab).

Non-drug treatment:

  • Diet: balanced and insisting on the polyunsaturated fatty acid intake to decrease inflammatory activity. Avoid obesity.
  • Exercise prevents contractures, muscle atrophy, decreased joint mobility and secondary prevention of osteoporosis.
  • Vaccination against pneumococcus (Streptococcus pneumoniae) and influenza virus (flu) for immune suppression secondary to treatment. If we do not vaccinate or give a booster dose might get the flu or pneumonia.
  • Bracing: for highly symptomatic phases can be convenient to keep the joint at rest by orthopedic mechanisms.
  • Rehabilitation: exercise therapy, electrotherapy, hydrotherapy, etc..
  • Surgery indicated for the treatment of intractable pain, for the correction of deformities and joint stabilization to prevent tendon ruptures, etc..

Bibliografía:

Rozman, C. Cardellach, F et al. Medicina Interna. 16 ed. Madrid: Elsevier; 2008.
Grupo GUIPCAR. Guía de práctica clínica para el manejo de la artritis reumatoide en España. Madrid: Sociedad Española de Reumatología; 2007. [En línea] [fecha de acceso: 14 de septiembre de 2011]. Disponible en: http://www.taiss.com/publi/absful/TAISS-abstract-GUIPCAR-esp-1.pdf
García Díaz, S. Educación para la salud y ejercicio del paciente con artritis reumatoide. Metas Enfermería, 2007. 10(4): 19-23.

Signed. Rafael Vazquez Godino
University Diploma in Nursing.

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