Rheumatoid arthritis Symptoms and Treatment

Rheumatoid arthritis Symptoms and Treatment

Rheumatoid arthritis is an autoimmune disease in which the immune system of the body attacks its own tissues- cartilage and joint linings. Rheumatoid arthritis is characterized by inflammation of the joints, which causes swelling, pain, and loss of function

Rheumatoid is a very common condition, with a prevalence of an approximately 1%

It is 3 to 5 times more common in women than in men

The peak incidence is in the second to fourth of life, but no age is immune.

Rheumatoid arthritis Pathogenesis

Normally, microbes are immunogenic, self-antigens tolerogenic (or ignored)

Breakdown of tolerance, which is multi-layered, consisting of central and peripheral mechanisms result in autoimmune reactions.

Failure of self-tolerance, which may occur because of intrinsic abnormalities in lymphocytes.

It is proposed that the disease is initiated in a genetically predisposed individual by activation of helper T cells responding to some arthritogenic agent, possibly microbial.

In turn, the activation CD4TH cells produce cytokines that will.

i) Activate macrophages and other cells in the joint space, releasing degradative enzymes and other cytokines (TNF and IL-1) that perpetuate inflammation and

ii) Activate ß cells, resulting in the production of antibodies, some of which are directed against self- constituents.

iii) Secondary activation of endothelium

The rheumatoid synovium is rich in both lymphocyte & macrophage-derived cytokines.

TNF ↑ the expression of adhesion molecules and endothelial cells, which result move cells to the joint.

TNF contributes to osteoclast activation and differentiation.

Interleukin (IL-1) mediates cartilage degradation directly by inducing the expression of MMP s by chondrocytes.

IL-1 & TNF induce synovial fibroblast to express cytokines, chemokines growth factors, and matrix metalloproteinases which contribute to cartilage and bone destruction.

Chemokines are secreted by macrophages and attract more cells into the joint.

The membrane then produces an abnormal granulation tissue, called pannus, that adheres to the surface of the articular cartilage and sometimes erodes the cartilage completely.

Autoreactive β cells can be driven by the T cells to produce IgG autoantibodies which result in the generation of rheumatoid factors (RF) which recognizes Fc of IgG.

Circulating RFS are relatively involved in many of the extra-articular manifestations of RA and joints RF also contributes to the inflammation reaction to that site.

RFS and IgG form immune complexes that fix complement, attract neutrophils and lead to tissue injury by a type III hypersensitivity reaction.

There are the elusive infectious agent or agents whose antigens activate T cells

Many candidates have been considered, but none has been conclusively proved.

Suspects include EBV, Borrelia species, Mycoplasma species, parvovirus & mycobacteria.

Although joint damage in RA is of immune origin and appears to occur in genetically predisposed individuals, the precise trigger that initiates this reaction is still unknown.

Rheumatoid arthritis Clinical presentation

The primary symptom of RA is inflammation of the synovial membrane.

If untreated, the membrane thickness and synovial fluid accumulate.

The resulting pressure cause pain and tenderness.

The membrane then produces an abnormal granulation tissue, called pannus, that adheres to the surface of the articular cartilage and sometimes erodes the cartilage completely.

When the cartilage is destroyed, fibrous tissue joins the exposed bone ends. the fibrous tissue ossifies and fuses the joint so that it becomes immovable the ultimate crippling effect of RA.

The growth of the granulation tissue causes the distortion of the fingers that characterizes the hands of RA sufferers.

Rheumatoid arthritis Non- specific signs and

Rheumatoid arthritis symptoms

  • Fever
  • Malaise
  • Arthralgias & weakness

Rheumatoid arthritis Diagnosis

Diagnosis supported by laboratory and other results

I) X-ray in early stages show bone demineralization and soft tissue swelling; later loss of cartilage and narrowing of joint spaces; & finally cartilage & bone destruction & erosion subluxations and deformities.

II) RF is positive in 75% to 80% of patients as indicated by a titer of 1:160 or higher.

III) Synovial fluid analysis shows ↑ volume turbidity but ↓ viscosity and elevated WBC count (often greater than 10,000/μ )

IV) Serum protein electrophoresis may show elevated serum globulin levels.

v) Erythrocyte sedimentation rate & c- reactive protein are elevated in 85-90% of patients.

VI) Complete blood count usually shows moderate anemia, slight leukocytosis, and thrombocytosis.

Rheumatoid arthritis Treatment

Treatment goals for rheumatoid arthritis are linked to medications used in managing diseases.

Medication to reduce pain & inflammation

1)NSAID’S – Eg : ibuprofen, naproxen, ketoprofen, piroxicam, diclofenac

2)Cox-2 inhibitor (only celecoxib)

3)low dose systemic corticosteroids (CS)

4)Intra-articular depot corticosteroids                                                                                                                                                                                                                        Medications to prevent disease progression & loss of joint junction.

1) Disease-modifying antirheumatic drug (DMAD) also called ”nonbiologic DMARDS” includes methotrexate (MTX), hydroxychloroquine (HCQ), azathioprine (AZA), sulfasalazine (SZ), and leflunomide.

2) Biologic agent

3) Other immunomodulatory, cytotoxic, and immunosuppressive drugs – eg. azathioprine, Cyclosporine A, rarely cyclophosphamide, and d- penicillamine.

OSTEOARTHRITIS (OA)

  • Osteoarthritis is a degenerative joint disease that is characterized by
  • Progressive damage to the articular cartilage
  • Thickening of subchondral bone & joint capsule.
  • Formation of osteophytes.
  • Mild synovitis
  • Commonly known as “wear and tear” arthritis joint disease is the most common disorder of joints.

Classification

1) Idiopathic OA:- There is no known underlying or predisposing cause.

2) Secondary OA:- Which is associated with predisposing factors as

  • -Trauma
  • -Repetitive stress (Occupational, sports)
  • -Congenital abnormality
  • -Metabolic disorder
  • -Endocrine disorder (DM, obesity)
  • Other bone/ joint disease
  • (Rheumatoid arthritis, gout)

Pathogenesis

-Articular cartilage is the major target of degenerative changes in osteoarthritis.

-Normal articular cartilage is strategically located at the end of bones to performs two functions.

1)Bathed in synovial fluid, it ensures virtually friction-free movement within joints.

2)In weight-bearing joints, it spread the load across the joint surface in a manner that allows the underlying bones to absorb shock and weight without being crushed.

-These functions require the cartilage to be elastic (i.e. to regain normal architecture after being compressed) & for it to have unusually high tensile strength.

These attributes are provided by the two major components of the cartilage a special type of collagen (type II) & proteoglycans both secreted by chondrocytes)

As is the case with adult bones, articular cartilage is not static; it undergoes a turnover in which “worn out” matrix components are degraded and replaced.

This balance is maintained by chondrocytes which not only synthesize the matrix but also secrete matrix-degrading enzymes.

Thus the health of the chondrocytes and their ability to maintain the essential properties of the cartilage matrix determine joint integrity.

In osteoarthritis, this process is disturbed by a variety of influences.

Perhaps the most important of these influences are aging and mechanical effects.

It is an occurrence in weight-bearing joints & an ↑ the frequency of the disease in conditions that predispose the joints to abnormal mechanical stresses such as obesity and previous joint deformity.

 Pathophysiology

OA develops due to an imbalance between the destruction &  synthesis of the articular cartilage, so the pathology of the disease shows both destructions and attempted repair of the joint.

Rheumatoid arthritis Clinical features

-Signs & symptoms of osteoarthritis develop very gradually & usually affect only one or few joints.

The joints commonly involved include the hips, knees, lower lumbar and cervical vertebrae, proximal and distal interphalangeal joints of the fingers. 1st carpometacarpal joints & 1st tarsometatarsal joints.

Common complaints include joint stiffness & deep aching pain, particularly in the morning.

Crepitus a cracking sound caused by exposed surfaces of bone rubbing against each other is often present in severe cases.

Some degree of joint swelling is common & small effusions may develop.

Heberden nodes, small osteophytes on the distal interphalangeal joints, are most often encountered in women with primary osteoarthritis.

Laboratory tests

No specific laboratory test

Aspirated synovial fluid (if obtained) : leukocytosis & high viscosity.

Other diagnostic tests

Radiologic evidence may be misleading

Radiographic changes may include

are often absent in early osteoarthritis joint-space narrowing, subchondral bone sclerosis, and osteophytes (with disease progression) gross deformity and effusions (late osteoarthritis).

Osteoarthritis treatment

Medications used for the treatment of osteoarthritis are:-

1)Analgesics :- Acetaminophen & NSAIDS

2)Glucosamine and chondroitin

3)Intra-articular therapy:- corticosteroids and hyaluronic acid (hyaluronan)

4)Opioid analgesic

5)Topical analgesics:- topical NSAIDS counter-irritant

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