Arthritis

seperator5
Arthritis
RHEUMATOID ARTHRITIS

Rheumatoid arthritis (RA) is the most common inflamma­tory arthritis, affecting from 0.5% to 1% of the general population worldwide arthritis doctor in Vadodara. Although RA is primarily considered a disease of the joints, abnormal systemic immune responses are evident and can cause a variety of extra-articular manifestations arthritis doctor in Vadodara.

The prime target of RA is the synovium considering its vascularity, with subsequent deposition of immune complexes. The cause is not known but few factors can trigger its occurrence, i.e., environmental (smoking, bacterial or viral infection) and in genetically susceptible individuals (HLA DR 4). Gender is another factor with Female : Male ratio being 3:1. Other most important risk factor could be hereditary involvement.

 

Classic presentation of rheumatoid arthritis is early morning stiffness, pain and swelling in small joints (feet and hands) which is followed later by larger joints (knee and shoulder) with a symmetric pattern, presence of autoantibodies in serum. Occasional cases may have asymmetric involvement as well as single joint disease (mono articular rheumatoid). Over the coarse of time, profuse synovial inflammation forms what is called Pannus, which is an inflamed granulation tissue that starts damaging the articular cartilage resulting in pain and deformity as shown in Fig.1.

 

Diagnosis is made with the typical presentation of multiple joint pain (particularly small joints), early morning stiffness, presence of Rheumatoid factor or Anti CCP in the serum and radiographic changes of arthritis.

The focus of treatment should be early diagnosis and to keep the disease activity at its low. The stream line of treatment comprises of DMARDS (disease modifying anti-rheumatoid drugs) which is used to combat RA is early stages with significant disease control.

Glucocorticoids pave way for the next line of treatment which rapidly controls the disease process. Recent development is the use of Biologic DMARDS like Anakinra, Rituximab and Abatacept which are infused to control multiple inflammatory mediators in patients not responding to the standard treatment protocol.

Patients with significant synovial hypertrophy (inflammation) of large joints like the knee will definitely benefit from Arthroscopic synovectomy which is considered the most important inflammatory producer. In advanced cases with significant joint erosions as in the knee, hip and shoulder, total joint replacement is the only available effective treatment which would improve the quality and life as well as render the patients pain free.

Arthritis1

 

SYMPTOMS

Symptoms of RA include:

  • Pain, Swelling, and Stiffness in more than one joint
  • Symmetrical joint involvement
  • Joint deformity
  • Unsteadiness when walking
  • A general feeling of being unwell
  • Fever
  • Loss of function and mobility
  • Weight loss
  • Weakness
VARIOUS OTHER FORMS OF ARTHRITIS DO EXIST WHICH ARE NAMELY

Gout (seronegative arthritis) in which an alteration in the protein metabolism resulting in either over production or reduced excretion of the by product – Uric Acid, which accumulates in small joints initially (great toe) and later may involve other joints. The normal serum uric acid is less than 5.7mg/dl in females and less than 7.7 mg/dl in males.

In aggressive case, uric acid crystal deposition in joints may cause excessive damage. Factors considered to cause gout are high protein diet, alcohol consumption, stress.

We are arthritis doctor in vadodara, arthritis doctor in baroda, arthritis treatment in vadodara, arthritis treatment in baroda

Gout can be effectively controlled with appropriate uric acid lowering diet, healthy lifestyle habits and uric acid lowering drugs such as Colchicine, Allopurinol, Febuxostat.

There is a separate entity of Arthropathy apart from gout which are considered seronegative arthritis which shows inflammatory markers in the serum without of presence of RF (Rheumatoid factor). These includes

  • Psoariatic arthritis caused secondary to skin disease, and appropriate treatment with steroids and controlling the infectious process will help control or suppress the arthritic process.
  • Ankylosing spondylitis which is spinal equivalent of Rheumatoid arthritis with cardinal features being involvement of axial skeleton especially the sacro-iliac joint, asymmetric peripheral joint involvement, usually associated with HLA B 27 gene, pain along tendon insertion (enthesopathy),with male preponderance.
  • Reactive arthritis
  • Juvenile Rheumatoid arthritis.

Appropriate diagnosis and early treatment of these conditions shall render a pain free and healthy life.

A complete ligament rupture requires the apposition of the divided ends followed by a period of protection if satisfactory healing is to be obtained. Depending on the situation, the injury may be treated conservatively by immobilization in a plaster – cast or, preferably, in a functional brace designed to allow joint movement whilst restricting the stresses on the healing ligament. If there is reason to doubt whether the torn ends are in apposition, the surgical suture may be advisable. Three weeks ’protection is usually sufficient to secure.

If time allows, it is usual to assess the situation
before surgery by angiography. With major vessels, the suture may be possible or the vessel may have to be repaired with a vein patch or a graft, usually taken from a vein. Fasciotomy is usually necessary.

numbness and muscular weakness developing later. The pain is typically made worse by stretching the affected muscles, which are also tender. Swelling of the ankle, foot, or hand is not necessarily a feature. Neurological signs eventually develop if the pressure is not released and in the late case the peripheral pulses may become impalpable. The presence or absence of the pulses is not, however, a good guide to the diagnosis.

Occasionally, following trauma to a limb, particularly a closed fracture or crush injury, the venous outflow from a fascial compartment may become obstructed by swelling, causing the pressure to rise gradually within the compartment. When the pressure reaches a critical level, any nerves passing through the compartment cease to function, initially causing paraesthesiae, followed by loss of sensation in the area supplied by the nerve. As the pressure continues to rise, tissue perfusion may cease, particularly in the muscles, and, rarely.