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Transcript of Rheumatoid arthritis dr.abdallah
RHEUMATOID ARTHRITIS (RA)
By:DR.ABDALLAH FAHEL
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RHEUMATOID ARTHRITIS (RA)
Gergely Péter dr
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 andultimately 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 1631Dutch 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-DR4In 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 feeding4-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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CytokinekinterakcióiCytokineinteractions
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Rheumatoid SynoviumRheumatoid Synovium
Normal SynoviumNormal Synovium Rheumatoid SynoviumRheumatoid Synovium
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Symptoms of Rheumatoid Arthritis:• Symptoms first begin in the small joints of the fingers, wrists and feet, with warm, swollenand 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 (suchas 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 atleast 6 weeks
2. Swelling of 3 or more joints for at least 6 weeks3. Swelling of wrist, metacarpophalangeal (MCP) or
proximal interphalangeal (PIP) joints for at least 6weeks
4. Symmetric joint swelling5. Typical radiologic changes in hands (erosions or
unequivocal bony decalcification)6. Rheumatoid nodules7. 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 & Cinfection)- 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)
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 onsetSlow development of sign & symptomsStiffnessPolyarticularMost common: PIP & MCP of handsMorning stiffness > 1hrFatigue, 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
Early assymmetric RA19
PIP joint involvement in RA20
RA: swan neck deformity21
RA: ulnar deviation22
Ulnar deviation in RA with severe atrophy of interossealmuscles 23
RA: Boutonnière deformity24
RA: arthritis mutilans25
Involvement of joints of feet in RA26
Severe destruction of ankles in RA27
Baker’s cyst28
Bursitis in the shoulder29
Bursitis and rheumatoid nodule30
Rheumatoid nodules31
RA – end stage32
Initial work-upCBC, 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
Radiology: X-Ray MRIBone Scan Symmetrical1-Early: no sig changes2-Late:
-Juxta-articular osteoporosis w/ decr bone density *Uniform jt narrowing.*Marginal erosions.
*Marginal cortical erosions *Juxtaarticular osteoporosis of lesser metsIll-defined ersosion of posteroanterior aspect of calcaneus
Resiters, PA, AS, hyperparathyroidism
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Periarticular osteoporosis (decalcification)35
Erosions and sclerosis (in late stage)36
Erosion in RA37
Early erosions (MRI)38
Scinti-graphy ofthe hands
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Atlantoaxialsubluxation
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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 ofRA:pulmonary fibrosis
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Interstitial pneumonitis in RA
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Systemic manifestations ofRA:Caplan’s syndrome
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Rheumatoid nodules in the lungs45
Episcleritis in RA46
Scleritis in RA47
Scleromalacia perforans
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Vasculitis in RA
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Vasculitis in RA50
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 andprevent joint damage.• Evaluation by a rheumatologist for the development and monitoring of a treatment plan isrequired in most people with RA.• Treatment plans often include a combination of rest, physical activity, joint protection, useof 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 reducejoint 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)Disease modifying antirheumatic drugs (DMARD): Drug Adverse effects Dosegold (i.m.) dermatitis, stomatitis, 25-50 mg /2-4
proteinuria, enterocolitis, weeksthrombocytopenia
gold (p.o.) less frequently used, brecause of lower tolerability
chloroquine (hydroxy- retinopathia, pigment- 250 mg/daychloroquine) anomalies
Regular ophthalmology check is requiredd-penicillamine proteinuria, myasthenia, 125-750 mg/day
stomatitisOwing to low tolerability it is not used any more
azathioprine hepatitis, bone marrow depression 50-150 mg/day
Scarcely given in RAmethotrexate hepatotoxicity, pulmonary fibrosis, 7,5-25 (MTX) bone marrow depression mg/week
most frequently used therapy 56
sulfasalazine nausea, vomiting 1,5-2 g/daydiarrhea, bone marrow depression
cyclosporine A nephrotoxicity, tremor 1,5-4 mg/kg/daycreatinine and blood pressure should bechecked regularly
leflunomide hepatotoxicity, GI 10-20 mg/daycomplaints
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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