Rheumatoid Arthritis Systemic chronic inflammatory disease Mainly affects synovial joints

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Rheumatoid Arthritis Systemic chronic inflammatory disease Mainly affects synovial joints Variable expression Prevalence about 3% Worldwide distribution Female:male ratio 3:1 Peak age of onset: 25-50 years

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Rheumatoid Arthritis Systemic chronic inflammatory disease Mainly affects synovial joints Variable expression Prevalence about 3% Worldwide distribution Female:male ratio 3:1 Peak age of onset: 25-50 years. Rheumatoid Arthritis. Unknown etiology Genetics Environmental - PowerPoint PPT Presentation

Transcript of Rheumatoid Arthritis Systemic chronic inflammatory disease Mainly affects synovial joints

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Rheumatoid Arthritis

Systemic chronic inflammatory disease

Mainly affects synovial joints

• Variable expression

• Prevalence about 3%

• Worldwide distribution

• Female:male ratio 3:1

• Peak age of onset: 25-50 years

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Rheumatoid Arthritis

• Unknown etiology

– Genetics

– Environmental

– Possible infectious component

• Autoimmune disorder

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THE PATHOLOGY OF RA

• Serositis

1. Synovitis

Joints

Tendon sheaths

Bursae

• Nodules

• Vasculitis

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Signs and Symptoms

• Joint inflammation– Tender, warm swollen joints– Symmetrical pattern

• Pain and stiffness• Symptoms in other parts of the body

– Nodules– Anemia

• Fatigue, occasional fever, malaise

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JOINT INVOLVEMENT ON PRESENTATION OF RA

Polyarticular 75% Monoarticular 25%

Small joints Knee 50%

of hands and feet 60%

Large joints 30% Shoulder }

Wrist }

Large and Hip } 50%

Small joints 10% Ankle }

Elbow }

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Articular features seen in the Rheumatoid Hand

WRIST: PIPs:

Synovitis Synovitis

Prominent ulnar styloid Fixed flexion or extension

Subluxation and collapse of deformities

carpus (Swan neck or boutonniere

Radial deviation deformity)

MCPs: THUMBS:

Synovitis Synovitis

Ulnar deviation ‘Z’ deformity

Subluxation

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Joint Destruction

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Extra-articular manifestations

• General– fever, lymphadenopathy, weight loss, fatigue

• Dermatologic– palmar erythema, nodules, vasculitis

• Ocular– episcleritis/scleritis, scleromalacia perforans,

choroid and retinal nodules

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Extra-articular manifestations

• Cardiac– pericarditis, myocarditis, coronary vasculitis,

nodules on valves

• Neuromuscular– entrapment neuropathy, peripheral

neuropathy, mononeuritis multiplex

• Hematologic– Felty’s syndrome, large granular lymphocyte

syndrome, lymphomas

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Extra-articular manifestations

• Pulmonary– pleuritis, nodules, interstitial lung disease,

bronchiolitis obliterans, arteritis, effusions

• Others– Sjogren’s syndrome, amyloidosis

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Investigations:

• Hematology : CBC , ESR

• Biochemistry : LFT , Renal profile

• Serology : RF , Anti-CCP

• Radiography : Joints , Spines ,Chest

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Treatment Goals

• Relieve pain

• Reduce inflammation

• Prevent/slow joint damage

• Improve functioning and quality of life

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Treatment Approaches

• Lifestyle modifications

• Rest

• Physical and occupational therapy

• Medications

• Surgery

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Rationale for the Early Treatment of R.A.

•Erosions develop early in the disease course•Destruction is irreversible•Disease activity is strongly associated with joint destruction later in the disease course•Early treatment can slow down radiographic progress•Disease activity must be suppressed maximally in its early stages to prevent destruction and preserve function

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Drug Treatments

• Nonsteroidal anti-inflammatory drugs (NSAIDs)

• Disease-modifying antirheumatic drugs (DMARDs)

• Biologic response modifiers

• Corticosteroids

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Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Traditional NSAIDs

• Aspirin • Ibuprofen • Ketoprofen• Naproxen

COX-2 Inhibitors

• Celecoxib• Rofecoxib

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Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

• To relieve pain and inflammation

• Use in combination with a DMARD

• Gastrointestinal side effects

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Disease-Modifying Antirheumatic Drugs (DMARDs)

• Hydroxychloroquine• Sulfasalazine• Methotrexate• Leflunomide• Gold• Azathioprine

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Disease-Modifying Antirheumatic Drugs (DMARDs)

• Control symptoms

• No immediate analgesic effects

• Can delay progression of the disease (prevent/slow joint and cartilage damage and destruction)

• Effects generally not seen until a few weeks to months

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DMARDs

• hydroxychloroquine– mild non-erosive disease– combinations– 200 mg bid– eye exams

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DMARDs

• Sulfasalazine– 1 gm bid - tid– CBC, LFTs– onset 1 - 2 months

• Methotrexate– most commonly used drug– fast acting (4-6 weeks)– po, SQ - weekly– CBC, LFTs

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DMARDs

• IM Gold– slow onset (3-6 months)– weekly then monthly injections– CBC, UA before each injection

• Oral Gold– less effective– slow acting (4-6 months)– daily– CBC, UA

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Biologic Response Modifiers

• Etanercept

• Infliximab

• Anakinra

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Biologic Response Modifiers

• Etanercept and infliximab target tumor necrosis factor alpha (TNF-)

• Anakinra targets interleukin-1 receptor

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OSTEOARTHRITIS

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MULTIFACTORAL ETIOLOGY OF OA

● Joint instability

● Age

● Hormonal factors

● Trauma

● Altered biochemistry

● Inflammation

● Genetic predisposition

● ? Others

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SYMPTOMS AND SIGNS OF OA• Pain – worse on use of joint• Stiffness – mild after immobility• Loss of movement• Pain on movement/restricted range• Tenderness (articular or periarticular)• Bony swelling• Soft tissue swelling• Joint crepitus

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RADIOLOGICAL FEATURES OF OA

• Narrowing of joint space

• Osteophytosis

• Altered bone contour

• Bone sclerosis and cysts

• Periarticular calcification

• Soft-tissue swelling

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MANAGEMENT OF OSTEOARTHTITIS

• Confirm diagnosis

• Initial Therapy :

Pysiotherapy

Wt loss

Local therapy

Paracetamol

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MANAGEMENT OF OSTEOARTHTITIScont

• Second-line approach:

NSAIDS

Intra-articular therapy: steroids,hyalurinate

Opioids

?glucosamines

Arthroscopy

Surgery

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