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rheumatoid arthritis
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RHEUMATOID ARTHRITISRHEUMATOID ARTHRITIS
Blondina Marpaung
Rheumatologi DivisionInterna Department
FK USU - Medan
Artritis Reumatoid :
widely spread , too all group, race, ethnic all the
world
Sistemic inflamatory autoimun deseases
Chornic inflamatory on joint
It’s a progresif poli artritis
Joint and other body organ
Symptom of chronic deseases
joint damaged deformitiy
disabilitity
Etiology sure ????
Autoimun Deseases :Autoimun Deseases :
Imune system activatedImune system activated
Attack the healty tissue Attack the healty tissue
Inflamation and tissue damage / organInflamation and tissue damage / organ
Autoimun process include :Autoimun process include :
T & B cell Messenger molecules Antibodi (RF) Anti cyclyc citrullinated C-peptic antibody (anti-CCP-ab) Type of cytokine
- Interleukin-1 (IL-1)
- Tumor necrosis factor (TNF- )
- Chemokin and the reseptor Signalling and co stimulatory molecules mast cell
SinoviocyteSinoviocyte Ectopic lymphoid neogenesisEctopic lymphoid neogenesis Angiogenesis Angiogenesis HLA-class IIHLA-class II Non-MHC risk genesNon-MHC risk genes Arthritogenic antigenArthritogenic antigen Macrofag Macrofag Dendrit cellDendrit cell Blys (B-lymphocytes stimulator)Blys (B-lymphocytes stimulator) APRIL (a proliferating inducing legand)APRIL (a proliferating inducing legand) SmokingSmoking Gender Gender
EpidemiologyEpidemiology Most commonly affect ~1% from populationMost commonly affect ~1% from population
Commonly on womanCommonly on woman
Onset of disease is usually between 40 and 50 Onset of disease is usually between 40 and 50
years of age, but can start at any ageyears of age, but can start at any age
Occurs in all races and ethnic groups, but is rare in Occurs in all races and ethnic groups, but is rare in
less developed and more rural parts of the worldless developed and more rural parts of the world
Etiology/PhatogenesisEtiology/Phatogenesis
Rheumatoid arthritis (RA) is chronic, inflamatory, Rheumatoid arthritis (RA) is chronic, inflamatory,
sistemic, autoimmune disease sistemic, autoimmune disease
Commonly polyarticular disease Commonly polyarticular disease
Chronic inflamation in sinovial membran dari from Chronic inflamation in sinovial membran dari from
affected jointaffected joint
Spesific cause of RA is unknown, but immune respon Spesific cause of RA is unknown, but immune respon
is characteristic well.is characteristic well.
PATHOGENESIS ETIOLOGY
Changes are:
Microvasculer destruction, oedem on sinovial tissue, lining proliferation cell on sinovial.
Tercell leukosit polimorfonuklear on sinovial. surface
Small vessel obliteration due to organized inflammation and
thrombus
Synovial fluid consist PMN leucocyte
Celluler Phatology
Tampak adanya :
synovial edem
Hyperplasia and hypertrophy lining cell sinovial can be thickening due to increasing A cell (reticuloendothelial
like) and B cell
Destroy Lysosom
Kapiler obstruction
Neutrophyl infiltration to artery wall
Thrombosis area
perivaskuler haemorrhage
DEGRADATION PROCESS
- Cartilage damage - ligament damage
- tendon damage - bone damage
proteoglycan thinning: - abnormal - not shiny
- not elastic
- not strong enough
Membrane synovial proliferation
Pannus : vaskular granulation tissue insist of
proliferation fibroblast
small vessel
inflammation cell
cauesd damage
Primer synovial disease,
Scunder synovial fluid,
cartilage, paraarticuler, tendon and
vascular component changes.
Clinical patternClinical pattern
Lipsky (1998); Wolfe (1996)
Progressive onset (from Progressive onset (from weeks to months)weeks to months)
Pain and stiffness Pain and stiffness (synovitis)(synovitis)
Swollen jointsSwollen joints Symmetric articular patternSymmetric articular pattern Flu-like symptomsFlu-like symptoms Morning stiffnessMorning stiffness FatigueFatigue
Clinical pattern (cont’d)Clinical pattern (cont’d)
At onset, RA usually affects hands, wrists At onset, RA usually affects hands, wrists and feetand feet
Often a chronic cyclical course Often a chronic cyclical course During flare-ups, new joints are affected During flare-ups, new joints are affected
and existing lesions are worsenedand existing lesions are worsenedJoints become deformed, leading to Joints become deformed, leading to
additional disabilityadditional disability
HANDS
• spindle shape finger- shape fusiform due to PIP swollen
• Swan neck deformity ( PIP hyperextention DIP flexion )
• Boutonniere deformity ( PIP flexion DIP extension)
• thumb :
- interphalanx joint hyperextension and MCP flexion
losss of clamp capacity thumb
Lateral deviation of the MCP jointsLateral deviation of the MCP joints
Slide 9
-Simetris play roles in RA difference from other arthritis
-DIP not include
morning stiffness can be used as disease severity
Wrist joint
( most common affected R.A)
* Boggy synovium
* ulnar swollen
* Impairment of wrist dorsoflexion
* Carpal-tunnel syndrome supressed N.Medianus tertekan)
ELBOW
* Contracture flexion
* Swollen
* para-olekranon destruction
* Joint dislokation
SHOULDER
* glenohumeralis joint
* Acromioclavicularis
* Thoracoscapularis
HIPHIP
( less affected R A)( less affected R A)
* abnormal gait
* Limited joint movement
* Inguional discomfort
KNEEKNEE
( most affected.RA( most affected.RA
* Hypertrophy sinovial
* Joint effusion
* quadricep muscle atrophy
* Baker cyst formation
(if cyst broken, signs like
thromboplebitis)
* Joint instability
LEGS AND ANKLE JOINT
• Limited flexion and extention
• Heel pain and bursa pain or pain in area under bursa of tendon Achiles and plantar pedis
• Hallux valgus (deviasion lateral of thumb food )
CERVICALCERVICAL
* Cervical Pain and stiffnes
* Progressive erosion
* Sub luxatio Atlanto axial. = Med. Spinalis compression neurologic sign = Artery vertebralts rotation and suppresion ( sinkope can occur when down a head )
* Local pain
* Muscle spasme limited rotated movement
* occipital pain
Extra-articular patternExtra-articular pattern
In some cases, RA has an extra-articular pattern In some cases, RA has an extra-articular pattern (involvement of other organ systems)(involvement of other organ systems)
Usually occurs in rheumatoid factor (RF)-positive Usually occurs in rheumatoid factor (RF)-positive patients with more severe articular diseasepatients with more severe articular disease
More common in menMore common in men
Vaskulitis
Lung disorder (Pleuritis, Pneumonitis)
Pericarditis
Nodul Rheumatic :- bursa olecranon
-upper arm external
- tendo Achilles
- ear
Neuropathy
Cornea and conjunctival lesion
Scleritis
Lymphe hypertrophy
splenomegaly
Hyperpigmentation
Skin ulcer
Lymfphadenopathy
Anemia
Thrombocytopenia
LABORATORYLABORATORY
* Increase BSR
* Mild Anemia ringan
* Rheuma factor :
Rose waaler more spesific / latex more sensitive.
* Factor APF most spesific
•Complete blood count, urine routin, renal and
liver function
* exudate synovial fluid
DiagnosisDiagnosisClinical patternClinical pattern
BiologyBiology
ImageryImagery
Biology Biology Elevation of common non-specific serum markers of Elevation of common non-specific serum markers of
inflammation contributes to the assessment of disease inflammation contributes to the assessment of disease activity levelactivity level
Erythrocyte sedimentation rate (ESR)Erythrocyte sedimentation rate (ESR) C-reactive protein (CRP)C-reactive protein (CRP)
Rheumatoid factors (RF)Rheumatoid factors (RF) Usually appear in the first year of the diseaseUsually appear in the first year of the disease ~80% of RA patients are RF+ (IgM the main isotype)~80% of RA patients are RF+ (IgM the main isotype) Associated with more rapidly evolving the more erosive Associated with more rapidly evolving the more erosive
disease and a higher incidence of extra-articular disease and a higher incidence of extra-articular manifestationsmanifestations
RF can be detected in healthy patients during infections (4% RF can be detected in healthy patients during infections (4% in Caucasians)in Caucasians)
RF also associated with other chronic diseases (1)RF also associated with other chronic diseases (1)
Imagery — conventional X-rayImagery — conventional X-ray
Performed at disease onset and on a regular basisPerformed at disease onset and on a regular basis Usually hands and feet; other joints monitored Usually hands and feet; other joints monitored
according to the disease patternaccording to the disease pattern Bone erosions and joint space narrowing patterns Bone erosions and joint space narrowing patterns
notednoted Approximately 30% of patients already have bony Approximately 30% of patients already have bony
erosion at disease onset (>60% at 2 years)erosion at disease onset (>60% at 2 years)
Common X-ray featuresCommon X-ray features
CaCCCage CaCCCage damage damage int int space narrowing)space narrowing)
Bone erosionBone erosion
Ultrasounds and MRIUltrasounds and MRI
Synovitis detection is mainly assessed Synovitis detection is mainly assessed clinicallyclinically
In difficult cases, ultrasound may be useful In difficult cases, ultrasound may be useful to detect synovitis and tenosynovitisto detect synovitis and tenosynovitis
MRI is not used in routine practiceMRI is not used in routine practice
Diagnostic criteria (ACR)Diagnostic criteria (ACR)
Presence of at least 4 of the following criteria: Presence of at least 4 of the following criteria:
Morning stiffness Morning stiffness 1 hour1 hour Arthritis of Arthritis of 3 of the following joints: right or left proximal 3 of the following joints: right or left proximal
interphalangeal (PIP), metacarpophalangeal (MCP), wrist, interphalangeal (PIP), metacarpophalangeal (MCP), wrist, elbow, knee, ankle and metatarsophalangeal (MTP) jointselbow, knee, ankle and metatarsophalangeal (MTP) joints
Arthritis of wrist, MCP or PIP jointArthritis of wrist, MCP or PIP joint Symmetric involvement of jointsSymmetric involvement of joints Rheumatoid nodules over bony prominences, or extensor Rheumatoid nodules over bony prominences, or extensor
surfaces, or in juxta-articular regionssurfaces, or in juxta-articular regions Positive serum RFPositive serum RF Radiographical changes, including erosions or bony Radiographical changes, including erosions or bony
decalcification localised in — or adjacent to — the involved jointsdecalcification localised in — or adjacent to — the involved joints
Rheumatoid Arthritis ( ACR, 1987 ) :
1. Morning stiffness minimal 1 hour, minimal for 6 weeks
2. Joint swollen in 3 or more for minimal 6 weeks3. Swollen in wrist, metacarpophalangeal or proximal interphalangeal joint for 6 weeks
4. simetric joint swollen
5. Characteristic radiology for RA in hands, includes unequivocal bone erosion and decalsification
6. rheumatoid nodul
7. Rheumatoid positif factor ( with healthy people (+) < 5 %)
Determine Diagnosis RA if 4 kriteria or more were found
Therapeutic goalsTherapeutic goals
Primary goals in the treatment of RAPrimary goals in the treatment of RAPrevention or control of structural damage to Prevention or control of structural damage to
jointsjointsPrevention or reversal of disabilityPrevention or reversal of disabilityPain reliefPain reliefTo improve quality of lifeTo improve quality of life
The ultimate goal is to achieve disease The ultimate goal is to achieve disease remissionremission
Treatment strategy approachesTreatment strategy approaches
Since the 1990sSince the 1990s Emphasis on limiting joint destructionEmphasis on limiting joint destruction Earlier use of intensive treatmentEarlier use of intensive treatment Methotrexate and sulfasalazine are considered Methotrexate and sulfasalazine are considered
first-choice DMARDsfirst-choice DMARDs Use of combination therapy including triple Use of combination therapy including triple
therapy in difficult disease (methotrexate, therapy in difficult disease (methotrexate, sulfasalazine, fractal signature analysis)sulfasalazine, fractal signature analysis)
ESTABLISHESTABLISHRA DIAGNOSISRA DIAGNOSIS EvaluateEvaluate
• Disease activity/extent of synovitisDisease activity/extent of synovitis• Structural damageStructural damage• Functional/psychosocial statusFunctional/psychosocial status
Initiate TreatmentInitiate Treatment• Patient educationPatient education• Physical and occupational therapy, etc.Physical and occupational therapy, etc.• NSAIDsNSAIDs• Possible local or oral steroids (Possible local or oral steroids ( 10 mg. Prednisone) 10 mg. Prednisone)
Assess Disease ActivityAssess Disease Activity
ACR GUIDELINES IN RA TREATMENTACR GUIDELINES IN RA TREATMENT
ACR GUIDELINES IN RA TREATMENTACR GUIDELINES IN RA TREATMENT
Remission or Satisfactory Control
Reactivation of Disease
Monitor Disease ActivityMonitor Disease ActivityPeriodicallyPeriodically
Assess Disease ActivityAssess Disease Activity
Start DMARDStart DMARDConsult RheumatologistConsult Rheumatologist
Monitor Disease ActivityMonitor Disease Activity
Revise Treatment PlanRevise Treatment Plan• Consult RheumatologistConsult Rheumatologist• Change NSAIDsChange NSAIDs• Change/add DMARDsChange/add DMARDs• Local or oral steroidsLocal or oral steroids• RehabilitationRehabilitation
Monitor Disease ActivityMonitor Disease Activity
Remission or Satisfactory Control
Spontaneous Remission (uncommon)
Persistent Active Disease
Persistent Active Disease
Reactivation of Disease
ACR GUIDELINES IN RA TREATMENTACR GUIDELINES IN RA TREATMENT
Refractory Rheumatoid ArthritisRefractory Rheumatoid ArthritisConsult RheumatologistConsult Rheumatologist• Most effective NSAIDMost effective NSAID• Most effective DMARDMost effective DMARD• Possible local or oral steroidsPossible local or oral steroids• RehabilitationRehabilitation
Persistent ActiveDisease
Monitor Disease ActivityMonitor Disease ActivityPeriodicallyPeriodically
Mechanical Joint Symptoms
Remission or Satisfactory Control
Reactivation of Disease
Surgical InterventionSurgical Intervention
Mechanical Joint Symptoms
Revise Treatment PlanRevise Treatment Plan• Consult RheumatologistConsult Rheumatologist• Change NSAIDsChange NSAIDs• Change/add DMARDsChange/add DMARDs• Local or oral steroidsLocal or oral steroids• RehabilitationRehabilitation
KlasifikasiKlasifikasiTreatment AR :Treatment AR : AnalgetikaAnalgetika Non steroidal anti inflamatory drugs (NSAID)Non steroidal anti inflamatory drugs (NSAID) Anti-rheumatic drugs Anti-rheumatic drugs
(SAARDs,DMARDs,TARTs)(SAARDs,DMARDs,TARTs) KortikosteroidKortikosteroid ImmunosuppresiveImmunosuppresive Gene therapy Gene therapy Biologicals agentBiologicals agent
• Journey of deseases uninfluence
• Reduce pain
• Using a months and waiting for remitif bioaviability
• Wacth out : gastritis, nausea ect
•Sistemik Steroid unrecommend to prevent
dependence and side-effect, except necesseary
SIMPTOMATIK DRUGSIMPTOMATIK DRUG : :
1. Analgetic : - salicylate (4-6 gr/hari) - paracetamol (1-2 gr/hari)
- codein (30 mg tiap 4 jam)
2. Anti inflamasi :
- aspirin ( 5 gr/ hari) - indomethasin (25-150 mg/hari)
- phenylbutazone (200-400 mg/hari)- oxyphenbutazone (200-400 mg/hari)
3. Corticosteroid :- Given for active and progresif pain- Minimal dose - Prednisone 10 -15 mg/hari- hydrocortisone asetate intra articular 20-50 mg
4. Anti inflamasi non steroid (NSAID)
- ibuprofen (600-1200 mg/hari) - naproxen (375-750 mg/hari)
- piroxicam (10-40 mg/hari) - profenid (100-600 mg/hari) - ketoprofen (100-200 mg/hari)
NSAID
• enzim cyclo-oxigenase supresed synthesa of prostaglandin.
• Possible stabilisation of membrane lysosomal
• Inhibit release activator mediator inflammation
• Inhibit cell migrasi to site of inflammation
• Inhibit selular proliferasi
• Neutralize free radical
• Generally potensial characteristic toxic
• Side Effect at gastrointestinal ( especially if combination with alcohol, smoking, stress, old age)
• Hipersensitif reaction
• Impairment liver function
• Impairment renal function
• Supressif of hematopoietik system
• Slow action waiting for blood level
Effec may occur 3-12 month later
• Side effect and high toksicity
• Expected to stop the progresifity/
become remission.
= Early joint destruction (90% RA erosion early 2 years.
= Result from worst therapy maybe because delay
DMARD
OBAT-OBAT REMITIF OBAT-OBAT REMITIF
DMADRSDMADRS
• Definite diagnose : DMARD immediately
• Suspect RA, respons NSAID minimal Start DMARD
• After using 3-6 month unsatisfied
Change with another DMARD
Combination
DMARD common use in AR Treatment
1. Klorokuin or hidroksiklorokuinm1. Klorokuin or hidroksiklorokuinm2. Sulfasalazine2. Sulfasalazine3. D-penisilamin3. D-penisilamin4. Garam emas4. Garam emas5. MTX5. MTX6. Siklosporin -A6. Siklosporin -A7. Leflunomide 7. Leflunomide
Gene therapyGene therapy Biological agentBiological agent
METHOTREXATE (MTX)METHOTREXATE (MTX)
• folat acid antagonis
• Reducing activity of thymidilate synthetase inhibisi 5-
aminoimidazole-carboximide-ribonucleotide transformylase
(AICAR) * IgM RF , IL-1 , IL-6
• 3 - 4 month action
• 7,5 mg per weeks (oral)
• 3 - 4 bulan no progress increase dose
for RA who progressive /fail with another DMARD
Side Effect MTX
• susceptible with infection
• nausea, vomitus, diare, stomatitis
• Impair Liver fuction
• alopesia
• aspermia
• lekopenia
-Leucovorin (folinat acid) 6 - 15 mg/m 2
6 hour during 72 hour, reduce side effect
MANAGEMENT OFRHEUMATOID ARTHRITIS
SOME DISEASE-MODIFYING ANTI-RHEUMATIC DRUGS (DMARDs)
DMARDMethotrexate
Hydroxychloroquine
Sulfasalazine
Leflunomide
Azathioprine
Cyclosporine
Gold
MONITORINGHematologic, liver, lung
Ophthalmologic
Hematologic, GI
Hematologic, liver
Hematologic, liver
Renal, blood pressure
Hematologic, renal
BIOLOGIC AGENTBIOLOGIC AGENT
= Biologic response modifiers = Targeted therapy
Anti tumor necrosis factor alpha / anti TNF- / TNF-blocked- ETANERCEPT (Enbrel)
anti soluble TNF receptor / sTNFR
anti cytokine therapy
- ADALIMUMAB (Humira)
- INFLIXIMAB (Renicade)
antibodi monoklonal
- RITUXIMAB (Mabthera)
depletion of B cells
Antagonis reseptor Interleukin- 1 (IL-1 ra) / blocking agent- ANAKINRA (Kineret)
Classification FUNCTIONAL CAPACITYClassification FUNCTIONAL CAPACITY (Steinbroke)
Class I : Complete Functional Capacity and able to do daily
activity with out trouble.
Class II: Functional Capacity Adequate daily activity with
dicomfort or limited movement on a joint or more
Class III: Functional Capacity for daily activity is limited.
Class IV: Nedd help with tool or person to do daily movement
PROGRESIFITY ClassificationPROGRESIFITY Classification(Steinbrocker)
Stage I, Early : 1. Without destruction on X-Ray
2. Osteoporosis maybe on X-Ray
Stage II, Moderate : 1. Osteoporosis, subchondrial bone and cartilage destruction
pada rontgent
2. Disturbing joint mobility without deformity
3.Appear of muscle atrophy
4. Nodule and tenosynovitis are finding
Stage III, Severe :
1. Cartilage and bone destruction beside osteoporosis
finding on X-Ray
2. Deformity like subluxation , ulnar deviation,
hyperextention without fibrosis or ankylosis
3. Explicit muscle atrophy
4. Nodulus and tenosynovitis are finding
Stage IV, Terminal :
1. Presence fibrous or ankylosis
2. Stage III criteria
KRITERIA UNTUK CLINICAL REMISSION :
1. Duration of morning stiffness less than 15 minute
2. Without fatique
3. Joint pain disappear
4. Disappear of pain and rigid movement
5. Swelling of joint tissue and tendon sheath
disappear
6. BSE less than 30 mm/hour (woman), 20 mm/jam man.
IF 5 from condition direct happen in 2 month , can mention remission reach out .
PSIKOTHERAPIPSIKOTHERAPI
( INFORMATION , SPIRIT , FAMILY SUPPORT)
-WHAT IS RA
-(Sistemic joint deseases, chronic, deseases progresivity
unestimate)
-, can spontaneus remission and relaps, and can be
deformity)
- MENTALLY READY
- DILIGENCE TO TAKE THE THERAPY AND ECCEPT THE TRUTH
PHYSICAL THERAPY :PHYSICAL THERAPY :• Joint position at most comfortable position
• Non acute process do mobilitation stage to prevent deformity
• Do not massage, symtomp will settle or increase
• Deformity prevent / flexion deformity
• Physiotherapy, occupational therapy, orthopedy,
phsicotherapy, social worker, phsichiatry, patient and family cooperation
• Auxillary tools : splint , stick , wheel chair,
special shoes, walking machine ect.
• Surgery : synovectomia, arthrodese, total hip ect.
DIETDIET
• Well Balanced : nutritious no specific food contra indication
• If the sign occurred iron def. :-ferros sulfat 0,2 gr, 3 x sehari /oral -follic acid
THANK YOU
Dr. Blondina Marpaung, SpPD - KR