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Rheumatoid arthritis(RA) : Etiology, Sign & symptoms, pathophysiology, diagnostic test, treatment

Rheumatoid arthritis|RA| Etiology of RA|

Sign&symptoms of RA|

pathophysiology of RA|Diagnostic test for RA|

Treatment of rheumatoid arthritis|

Can RA be cured?

Nonpharmacological therapy of RA|

Foods to avoid with RA|

pharmacological therapy of RA| 


Rheumatoid arthritis(RA):

Rheumatoid arthritis
Rheumatoid arthritis

• Rheumatoidarthritis (RA) is a systemic disease characterized by symmetrical inflammation of joints, yet may involve other organ systems.

• Control of inflammation is the key to slowing or preventing disease progression as well as managing symptoms.

• Drug therapy should be only part of a comprehensive program for patient management,which would also include physical therapy, exercise, and rest. Assistive devices and orthopedic surgery may be necessary in some patients.

• Patients should be treated to target of low disease activity or remission.

• Traditional or conventional synthetic disease-modifying antirheumatic drugs (referred to as DMARDs) should be started as soon as possible after diagnosis of RA.

• Nonsteroidal anti-inflammatory drugs (NSAIDs) and/or corticosteroids should be considered adjunctive therapy early in the course of treatment and as needed if symptoms are not adequately controlled with DMARDs or biologic DMARDs (referred to as biologics).

• When DMARDs used alone are ineffective or not adequately effective, other monotherapies
or combination therapy with two or more DMARDs or a DMARD plus biologic agent may be used to induce a response.

• Patients require careful monitoring for toxicity and therapeutic benefit for the duration of treatment.

• Rheumatoid arthritis (RA) is the most common systemic inflammatory disease characterized by symmetrical joint involvement. Extra-articular involvement, including rheumatoid nodules, vasculitis,eye inflammation, neurologic dysfunction, cardiopulmonary disease, lymphadenopathy, and splenomegaly, can be manifestations of the disease. Although the usual disease course is chronic,some patients will enter a remission spontaneously.

Etiology of RA:

Rheumatoid arthritis is a auto immune disease, which do not occur in racing population, aging population, due to physical stress on joint. It also doesn't occurs in sports players and due to injury. RA occurs in people who have genetic history, their father or mother had rheumatoid arthritis.

Sign & symptoms of RA:

• Joint pain and stiffness of more than 6 weeks’ duration. May also experience fatigue, weakness,low-grade fever, loss of appetite. Muscle pain and afternoon fatigue may also be present. Joint deformity is generally seen late in the disease.

• Tenderness with warmth and swelling over affected joints usually involving hands and feet.Distribution of joint involvement is frequently symmetrical. Rheumatoid nodules may also be present.
Rheumatoid arthritis

Pathophysiology of RA:

• RA results from dysregulation of humoral and cell-mediated immunity. Most patients produce antibodies called rheumatoid factors; these seropositive patients tend to have a more aggressive course than seronegative patients.

• Immunoglobulins (Ig) activate the complement system, which amplifies the immune response by enhancing chemotaxis, phagocytosis, and release of lymphokines by mononuclear cells that are then presented to T lymphocytes. Processed antigen is recognized by the major histocompatibility complex proteins on the lymphocyte surface, resulting in activation of T and B cells.

• Tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and IL-6 are proinflammatory cytokines important in initiation and continuance of inflammation.

• Activated T cells produce cytotoxins and cytokines, which stimulate further activation of inflammatory processes and attract cells to areas of inflammation. Macrophages are stimulated to release prostaglandins and cytotoxins. T-cell activation requires both stimulation by proinflammatory cytokines as well as interaction between cell surface receptors, called costimulation. One such costimulation interaction is between CD28 and CD80/86.

• Activated B cells produce plasma cells, which form antibodies that, in combina￾tion with the complement system, result in accumulation of polymorphonuclear leukocytes. These leukocytes release cytotoxins, oxygen-free radicals, and hydroxyl radicals that promote damage to synovium and bone.

• Signaling molecules are important for activating and maintaining inflammation. Janus kinase (JAK) is a tyrosine kinase responsible for regulating leukocyte maturation and activation. JAK also has effects on production of cytokines and immunoglobulins.

• Vasoactive substances (histamine, kinins, prostaglandins) are released at sites of inflammation, increasing blood flow and vascular permeability. This causes edema,warmth, erythema, and pain, and facilitates granulocyte passage from blood vessels to sites of inflammation.

• Chronic inflammation of synovial tissue lining the joint capsule results in tissue proliferation (pannus formation). Pannus invades cartilage and eventually the bone surface, producing erosions of bone and cartilage and leading to joint destruction.
End results may be loss of joint space and joint motion, bony fusion (ankylosis), joint subluxation, tendon contractures, and chronic deformity.

Diagnostic test for RA:

• Rheumatoid factor (RF) detectable in 60% to 70%.

• Anticyclic citrullinated peptide (anti-CCP) antibodies have similar sensitivity to RF (50%-85%) but are more specific (90%-95%) and are present earlier in the disease.

• Elevated ESR and CRP are markers for inflammation.

• Normocytic normochromic anemia is common as is thrombocytosis.

Other Diagnostic Tests:

• Joint fluid aspiration may show increased white blood cell counts without infection, crystals.

• Joint radiographs may show periarticular osteoporosis, joint space narrowing, or erosions.

Can RA be cured

Rheumatoid arthritis can not be cured as it is genetic disease but progression of diseases can be prevent by giving symptomatic treatment.

Treatment:

Non pharmacological therapy:

• Rest, occupational therapy, physical therapy, use of assistive devices, weight reduction, and surgery are the most useful types of non pharmacologic therapy used in patients with RA.

• Rest is an essential component of a non pharmacologic treatment plan. It relieves stress on inflamed joints and prevents further joint destruction. Rest also aids in alleviation of pain. Too much rest and immobility, however, may lead to decreased range of motion and, ultimately, muscle atrophy, and contractures.

• Occupational and physical therapy can provide the patient with skills and exercises necessary to increase or maintain mobility. These disciplines may also supply patients with supportive and adaptive devices such as canes, walkers, and splints.

• Other nonpharmacologic therapeutic options include weight loss and surgery. Weight reduction helps alleviate stress on inflamed joints. Tenosynovectomy, tendon repair, and joint replacements are surgical options for patients with RA. Such management is reserved for patients with severe disease.

Food to avoid with RA

There is no specific food to avoid with RA.

Pharmacological therapy of RA:

• Start disease-modifying antirheumatic drugs (DMARDs) as soon as possible after disease onset because early treatment results in more favorable outcomes.

• DMARDs slow RA disease progression. Common nonbiologic DMARDs include methotrexate (MTX), hydroxychloroquine, sulfasalazine, and leflunomid. The order of selection is not clearly defined, but MTX is often chosen initially because long-term data suggest superior outcomes compared with other DMARDs and lower cost than biologic agents.

• Combination therapy with two or more non-biologic DMARDs may be effective when single-DMARD treatment is unsuccessful. Recommended combinations include (1)MTX plus hydroxychloroquine, (2) MTX plus leflunomide, (3) MTX plus sulfasalazine, and (4) MTX plus hydroxychloroquine plus sulfasalazine.

• Biologic DMARDs include the anti-TNF agents etanercept, infliximab, adalimumab, certolizumab, and golimumab; the costimulation modulator abatacept; the IL-6 receptor antagonist tocilizumab; and rituximab, which depletes peripheral B cells. Biologic DMARDs have proven effective for patients failing treatment with nonbiologic DMARDs.

Anti-TNF biologics may also be used in patients with early disease of high activity and poor prognostic factors, regardless of previous DMARD use. Features of poor prognosis include functional limitation, extra-articular disease (eg, rheumatoid nodules, vasculitis) positive rheumatoid factor or ACPA, or bone erosions. Anti-TNF biologics canbe used as either monotherapy orin combination with other DMARDs.Use of biologics in combination with MTX is more effective than biologic monotherapy.

• DMARDs less frequently used include anakinra (IL-1 receptor antagonist), azathioprine, penicillamine, gold salts (including auranofin), minocycline, cyclosporine, and cyclophosphamide. These agents have eitherless efficacy or higher toxicity, or both.

• Nonsteroidal anti-inflammatory drugs (NSAIDs) and/or corticosteroids may be used for symptomatic relief if needed. They provide relatively rapid improvement compared with DMARDs, which may take weeks to months before benefit is seen.
However, NSAIDs have no impact on disease progression, and corticosteroids have potential for long-term complications.