+ All Categories
Home > Health & Medicine > Rhematoid arthiritis

Rhematoid arthiritis

Date post: 18-Aug-2015
Category:
Upload: jasleenbrar03
View: 9 times
Download: 1 times
Share this document with a friend
47
RHEUMATOID ARTHRITIS PRESENTED BY- JASLEEN KAUR BRAR
Transcript

RHEUMATOID ARTHRITISPRESENTED BY-

JASLEEN KAUR BRAR

INTRODUCTION

Rheumatoid arthritis is an auto immune disease that is caused by chronic inflammation of the joints or in the membrane surrounding the joints (the synovial membrane)

DEFINITION Rheumatoid arthritis (RA) is a chronic,

systemic autoimmune disorder whose major distinctive feature is chronic, symmetrical and erosive inflammation of the synovial tissue of the joints.

The severity of the joint disease may fluctuate over time, but progressive development of various degrees of joint destruction, deformity and disability is the most common outcome of established disease.

INCIDENCE

• About 1% of the world’s population is afflicted by rheumatoid arthritis.

• Onset is most frequent between the ages of 20 and 40, but people of any age can be affected.

• Women are three times more likely to get RA than men, however women who are taking or have taken oral contraceptives are less likely to develop RA.

ETIOLOGY• Rheumatoid factor (RF), an

autoantibody directed against immunoglobulin G (IgG)

• Antibodies against collagen, Epstein-Barr virus, encoded nuclear antigen

• Antikeratin antibody (AKA) & anti-perinuclear factor (APF)

RISK FACTORSGenetic factors- People with RA are more

likely to have a gene called HLA- DR4, located on chromosome 6.

Environmental factors- Infectious agents that may induce RA are mycoplasma organisms, Epstein-Barr virus, rubella virus and Streptococcus. Smoking is also a major environmental risk factor.

Hormonal factors- During pregnancy, women often experience a symptom improvement of RA, due to increase in estrogen and progesterone levels.

• The pathologic process involved in RA are type 3( immune complex) and type 4( cell mediated) reactions. If unarrested, pathologic changes in RA pass through four stages:

1. Synovitis2. Pannus formation3. Fibrous ankylosis4. Bony ankylosis

PATHOPHYSIOLOGY

Presentation of antigen to T cell

T and B cell proliferation

Activation of complement systemActivation of complex system &

release of lysosymes from leukocytes

Proliferative inflammation localized in joint capsule

Tissue thickens with edema and congestion

SYNOVITIS

STAGE 1

PANNUS gradually develops

Extends over the articular surface into joint anterior

Adheres tightly to underlying cartilage by invasion and lysis

Interferes with cartilage nutrition

Pannus may extend over to subchondral bone

Cartilage may become worn off and become raw

STAGE 2

Subchondral bone erosion

Granulation tissue gets invaded with tough fibrous tissue

Converted to scar tissue

Inhibits joint movements

Forms FIBROSIS ANKYLOSIS

Progress to bony ankylosis

STAGE 3

STAGE 4

CLINICAL MANIFESTATIONS

1.Articular Manifestations

2.Extra Articular Manifestations

ARTICULAR MANIFESTATIONS

Early stages –Active inflammation of jointsHot, swollen and painful joints

and function may be decreasedSoft tissue deformity and

contractures due to prolonged immobilization

Stiffness especially on first wakening in the morning

Later stages-Deformity of hands and feet

due to misalignment resulting from swelling, progressive joint destruction or partial dislocation.

Muscle spasm and weakness

Others –FeverRheumatoid nodules at joint capsulesFatigueWeaknessAnorexiaWeight lossGeneralized aching

Rheumatoid nodules•Subcutaneous•few millimetres to a few centimetres in diameter•usually found over bony prominences

Hand DeformitiesULNAR DRIFT

• Deviation of the MCP (metacarpophalangeal) joints of the fingers and medial deviation of the wrist.

• Most marked in the little finger and involves each successive finger to a lesser degree.

SWAN NECK DEFORMITY

• Hyperextension of PIP (proximal interphalangeal) joint with flexion of the MCP and DIP (distal interphalangeal) joints.

• Results from contractures of the intrinsic muscles and tendons.

THE BOUTONNIERE DEFORMITY

• Flexion of the PIP joints and hyperextension of the DIP joints.

• Due to rupture of the extensor tendons over the fingers.

EXTRA ARTICULAR MANIFESTATIONS

Vasculitis:digital arteritis fever, skin lesionschronic leg ulcersperipheral neuritisnecrotizing arteritis involving coronary,

mesenteric or renal vessels.

Serositis: Lungs- Fibrosis of the lungsPleural effusionsHeart- Prone to atherosclerosis, Risk of myocardial infarction & stroke Others: pericarditis, endocarditis, left

ventricular failure, valvulitis and fibrosis.

Eye- keratoconjunctivitis siccaNervous system- Peripheral neuropathy Carpal tunnel syndrome caused by

compression of the median nerve by swelling around the wrist.

Anemia

DIAGNOSTIC TESTS

Radiologic examination-• This consists of X rays of both hands and

of the affected joints. The following features may be present:

• Reduced joint space• Erosion articular margins• Subchondral cysts• Soft tissue swelling

Blood tests-• Elevated ESR • Decreased Hb value• Positive test for C reactive protein• ANA (antinuclear antibodies) – seen

in 15-20% clients• Rheumatoid factor (RF)- It can be

detected in serum by following tests:

• Latex fixation test- positive in titre 1:20

• Rose- waaler test – agglutination test sheeps RBC are used as carrier.

Synovial fluid examination-

• Arthroscopic examination shows synovial fluid is cloudy, milky or dark yellow

• contains numerous inflammatory components

• reduced viscosity • WBC count is as high as

50,000/mm3

Diagnostic Criteria

1. Morning stiffness of >1 hour most mornings for at least 6 weeks.

2. Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups, present for at least 6 weeks

3. Swelling of atleast 1 wrist, MCP, or PIP joint, present for at least 6 weeks

4. Symmetric arthritis, present for at least 6 weeks

5. Subcutaneous nodules in specific places

6. Presence of Rheumatoid factor 7. Radiological changes suggestive of

joint erosion four or more of the seven criteria must

be met before the disease is classified as RA.

TREATMENT

The aims are-

• The induction of remission and its maintenance: the disease’s activity is brought under control by drugs.

• The preservation of joint functions and prevention of deformities: during the activity of disease and thereafter by physiotherapy and splinting.

• Repair of the joint damage which already exists: it will relieve pain or facilitate functions. It sometimes requires surgical interventions eg. Synovectomy.

METHODS OF TREATMENT

MEDICAL MANAGEMENT

ORTHOPAEDIC MANAGEMENT

Medical Management

It has 3 goals:• Prevention of joint deformity• Preservation of joint function• Reduction of inflammation and pain.

It consists of• Rest• Physical therapy (isometric exercises)• Hot and cold application (moist, dry

heat, cold packs)• Diet

• Drugs Drugs like NSAID’sDisease Modifying Anti-

Rheumatic Drugs(DMARD’s)SteroidsNever massage acutely

inflamed joint.

Pharmacological management

• Aspirin / sodium salicylate: They are analgesic, anti-

inflammatory, relatively safe and inexpensive.

Analgesia is achieved in small doses and large doses are needed to reduce inflammation.

Frequent doses (3 to 4 times) are required, even when pain is not present to keep blood salicylate level high.

• NSAID’s: if aspirin is ineffective NSAID’s are given.

They are anti – inflammatory, analgesics and antipyretics e.g.

Phenylbutazone Indomethacin Ibuprofen* to be taken with histamine receptor

antagonist.

• CorticosteroidsWysolonePrednisolone• Intra- articular injections of

corticosteroids• Immunosuppressive (cytotoxic)

agents: Methotrexate,acts as an immunosuppresent, blocking the inflammatory process of RA.

Dietary management• No particular dietary

modification is required.• The client is encouraged to

eat a nutritious diet rich in vitamins, proteins, iron.

• If client is overweight, they are taught to loose weight to relieve stress on affected joints.

Orthopaedic management

• Tendon transfers and osteotomy:

Prevents progressive deformity which would be caused by muscle spasm.

Nodules or bony tumors can be surgically removed.

Osteotomy may improve the function of deformed joints or limbs.

• Synovectomy: It helps in maintaining

joint functions.Early surgical removal of

the synovium helps prevent recurrent inflammation.

• Joint replacement: eg. Arthrodesis or

arthroplasty( with or without replacement of joint parts with prosthesis).

Arthrodesis( fusion) sacrifices function of the joint but relieves pain in severely damaged joints.

Fusion may be performed on the wrists to fix affected part in a functional position so it can be used more effectively.

• Arthrodesis – surgical fusion of

joints

• Hip arthroplasty: both joint component is replaced

• Hemi arthroplasty: only one joint component is replaced eg. Replacement of head of femur with metal prosthesis.

Thus the surgerical management is divided into:

• Preventive surgery: eg synovectomy• Palliative surgery: for relief eg tendon

transfer• Reconstructive surgery: for

rehabilitation eg. Arthroplasty, total joint replacement


Recommended