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RHEUMATOID ARTHRITIS (RA) By: DR.ABDALLAH FAHEL 1
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Page 1: Rheumatoid arthritis dr.abdallah

RHEUMATOID ARTHRITIS (RA)

By:

DR.ABDALLAH FAHEL

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Page 2: Rheumatoid arthritis dr.abdallah

RHEUMATOID ARTHRITIS (RA)

Gergely Péter dr

Definition: Chronic destructive of joint inflammation

with pain and swelling,mainly characterized by

inflammation of the lining( synovium) of the joints .In a

considerable proportion of patients, the arthritis is

progressive, resulting in joint destruction and

ultimately incapacitation and increased mortality.

Relatively common,

prevalence: 0.3-1.5 %

, the male:female ratio cca. 1:3.

Typical case: woman aged 30-40 years with polyarthritis

and early joint deformities.

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History of Rheumatoid Arthritis

1858 – Dr Alfred Baring Garrod, named the condition Rheumatoid Arthritis.

1895 – X-Ray was discovered.

1912 – Dr. Frank Billings introduced the concept of focal infection.

In the 1920’s, physicians suspected the cause of RA was bacterial infection, they used gold and malaria drugs.

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RA in European Art

Dutch Priest 1631

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Wheelchair bound

w/ classic RA in his

hands

Renoit in 1911

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Etiology :1-gentic factor : may be involved because it is usually

associated with HLA-DR4

In white people and DR1 in indo-pak.

2-autoimmunity: RA is considered to be an

autoimmune disease for the following reasons:

*autoantibodies are present .

*immune comlex are common in synovial

Fluid.

There is defect in cell mediated immunity .

3-female gender: is a risk factor and this susceptibility

is increased post-partum and by breast feeding

4-cigarette smoking : is also a risk factor

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Pathogenesis :.

Is a disease of the synovium.

*inflammation :the synovium shows signs of chronic

inflammation .there swilling and congestion of synovial

membrane , and the underlying connective tissue which

becomes infilterated with lymphocyte,plasma cells and

macrophages .

*proliferation : the synovial membrane then proliferates and

grows out over the surface of the cartilage, which causes

erosion and destruction of the cartilage .

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Cytokinek

interakciói

Cytokine

interactions

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Rheumatoid Synovium

Normal Synovium Rheumatoid Synovium

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Symptoms of Rheumatoid Arthritis:

• Symptoms first begin in the small joints of the fingers, wrists and

feet, with warm, swollen

and tender joints that are painful and difficult to move.

• Joints of both sides of the body (symmetrical) are typically

affected.

• People with RA often experience fatigue, loss of appetite and

low-grade fever.

• There is often stiffness in the morning that lasts for several hours

or more.

• Nodules may form under the skin, often over the bony areas

exposed to pressure (such

as the elbows).

• Over time, damage to the cartilage and bone of the joints may

lead to joint deformities.

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Classification criteria of RA (ARA, 1987)

1. Morning stiffness – for at least 1 hr and present for at

least 6 weeks

2. Swelling of 3 or more joints for at least 6 weeks

3. Swelling of wrist, metacarpophalangeal (MCP) or

proximal interphalangeal (PIP) joints for at least 6

weeks

4. Symmetric joint swelling

5. Typical radiologic changes in hands (erosions or

unequivocal bony decalcification)

6. Rheumatoid nodules

7. Serum rheumatoid factor (RF) positivity

Diagnosis is made by the presence of 4 or more criteria

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Differential diagnosis of polyarthritis

RA should be differentiated from:

- Other autoimmune diseases (SLE, primary Sjögren’s syndrome,

MCTD, PM/DM, PSS, PAN, gian cell vasculitis, polymyalgia rheumatica,

adult onset Still’s disease)

- Viral diseases (parvovirus B19 infection, rubella, hepatitis B & C

infection)

- Bacterial infections (tbc, rheumatic fever, Jaccoud’s arthritis, septic

endocarditis, mycoplasma arthritis)

- Seronegative spondylarthritides (erosive psoriatic arthitis, reactive

arthritis, enteropathic arthritis)

- Paraneoplastic arthritis

- Other diseases (e.g. hyperthrophic osteoarthropathy, erythema

nodosum, agammaglobulinemia, acromegaly, diabetes mellitus)

- Other rheumatic diseases (chronic gout, inflamed erosive

osteoarthritis)

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Signs of early RA

(=undifferentiated arthritis)

In the early stage (within the first 3-6 months) (ARA)

classification criteria cannot be used.

The patient should be referred to a rheumatologist, if

• the patient has 3 or more swollen joints

• the metacarpophalangeal (MCP) and/or

metatarsophalangeal (MTP) joints are

involved; the squeeze test is positive

• morning stiffness is 30 min or more.

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How to diagnose a case of

RA?HISTORY:

Insidious onset

Slow development of sign & symptoms

Stiffness

Polyarticular

Most common: PIP & MCP of hands

Morning stiffness > 1hr

Fatigue, malaise, depression

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Squeeze test

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Joint involvement in RA

The most specific sign of RA is arthritis.

It is progressive and deforming in the

majority (2/3) of cases (= erosive

polyarthritis)

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RA early stage18

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Early assymmetric RA19

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PIP joint involvement in RA

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RA: swan neck deformity21

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RA: ulnar deviation22

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Ulnar deviation in RA with severe atrophy of interosseal

muscles 23

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RA: Boutonnière deformity24

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RA: arthritis mutilans25

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Involvement of joints of feet in RA26

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Severe destruction of ankles in RA27

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Baker’s cyst28

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Bursitis in the shoulder29

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Bursitis and rheumatoid nodule30

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Rheumatoid nodules31

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RA – end stage32

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Initial work-up

CBC, Metabolic panel, Urinalysis,

Rheumatoid factor, Anti-nuclear antibody.

Chem: nl, slight decr albumin, incr total

protein.

Hema:hemocrit- ACD, wbc- mildly up,

platelet- rare thrombocytosis

Laboratory Tests

ESR: elevated33

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Radiology:X-Ray

MRI

Bone Scan

Symmetrical

1-Early: no sig changes

2-Late:-Juxta-articular osteoporosis w/ decr bone density

*Uniform jt narrowing.

*Marginal erosions.*Marginal cortical erosions*Juxtaarticular osteoporosis of lesser mets

Ill-defined ersosion of posteroanterior aspect of calcaneusResiters, PA, AS, hyperparathyroidism

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Periarticular osteoporosis (decalcification)35

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Erosions and sclerosis (in late stage)36

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Erosion in RA37

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Early erosions (MRI)38

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Scinti-

graphy of

the hands

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Atlantoaxial

subluxation

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Extraarticular manifestations of RA

• rheumatoid nodules – subcutaneous

- in internal organs (lung,

aortic valve)

• pleuritis/pericarditis

• fibrotizing alveolitis

• Felty’s syndrome

• vasculitis

• amyloidosis

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Systemic

manifestations of

RA:

pulmonary fibrosis

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Interstitial pneumonitis in RA

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Systemic

manifestations of

RA:

Caplan’s syndrome

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Rheumatoid nodules in the lungs

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Episcleritis in RA46

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Scleritis in RA47

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Scleromalacia perforans

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Vasculitis in RA

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Vasculitis in RA50

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Leg ulcers in Felty’s

syndrome

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Large granular lymphocytes in Felty’s syndrome

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What is “Quality of Life”?

• Ability to

– Work

– Be a parent

– Socialize with others

– Exercise and be mobile

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Management of Rheumatoid Arthritis:

• The goals of treatment of RA are to reduce joint pain and

swelling, relieve stiffness and

prevent joint damage.

• Evaluation by a rheumatologist for the development and

monitoring of a treatment plan is

required in most people with RA.

• Treatment plans often include a combination of rest, physical

activity, joint protection, use

of heat or cold to reduce pain, and physical or occupational

therapy.

• Maintain a healthy body weight and maintain a physical activity

plan (i.e. Arthritis

.

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• Drugs play a very important role in the treatment of RA.

• Many people with RA take nonsteroidal anti-inflammatory drugs

(NSAIDs) to help reduce

joint pain, stiffness and swelling.

• Low doses of corticosteroids such as prednisone may also be

used to relieve joint pain,

stiffness and swelling and to reduce the risk of joint swelling.

• People with RA are often treated with disease-modifying anti-

rheumatic drugs

(DMARDs), such as methotrexate or leflunomide

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Disease modifying antirheumatic drugs (DMARD):

Drug Adverse effects Dose

gold (i.m.) dermatitis, stomatitis, 25-50 mg /2-4

proteinuria, enterocolitis, weeks

thrombocytopenia

gold (p.o.) less frequently used, brecause of lower

tolerability

chloroquine (hydroxy- retinopathia, pigment- 250 mg/day

chloroquine) anomalies

Regular ophthalmology check is required

d-penicillamine proteinuria, myasthenia, 125-750 mg/day

stomatitis

Owing to low tolerability it is not used any more

azathioprine hepatitis, bone marrow depression 50-150

mg/day

Scarcely given in RA

methotrexate hepatotoxicity, pulmonary fibrosis, 7,5-25

(MTX) bone marrow depression mg/week

most frequently used therapy 56

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sulfasalazine nausea, vomiting 1,5-2 g/day

diarrhea, bone marrow depression

cyclosporine A nephrotoxicity, tremor 1,5-4 mg/kg/day

creatinine and blood pressure should be

checked regularly

leflunomide hepatotoxicity, GI 10-20 mg/day

complaints

TNF- blockers: local reaction, autoimmune disease (SLE, SM)

(etanercept, infection (tbc)

infliximab, and

abatacept)

etanercept: 25 mg 2x weekly s.c.

infliximab: 3 mg/kg every 8 week i.v.

Other:

anakinra (IL-1 blocker)

rituximab (anti-CD20 antibody)

abatacept (T cell activation blocker antibody)

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THANK YOU

DR.ABDALLAH FAHEL

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