2. KEY PHYSICAL EXAM FINDINGS IN JOINT PAIN
ARTRICULAR (JOINT) DISEASE PERIARTRICULAR/ SOFT TISSUE
PHYSICAL EXAM OA Inflammatory
arthritis
Arthralgia Bursitis or
tendinitis
Myofascial
Swelling varies yes no yes no
Erythema no varies no yes no
warmth no yes no yes no
Tenderness Joint line yes varies periarticular yes
ROM limited limited Full or limited Full, often
limited by pain
full
Pain with active/
passive
both both Usually both Active > passive Usually both
3. Duration
acute (days)
Infection (bacterial/viral)
Trauma/ hematrosis
Crystal induced
Early chronic cause
Chronic (wks-mos)
Inflammation
Yes
Joint involved
mono
crystal induced
Poly
RA
SLE
Systemic vasculitis
Crystal induced
NO
OA
Tumor
4. COMPARISON OF MAJOR ARTHRITIDES
FEATURE OA RA GOUT/ CPPD (Calcium
Pyrophosphate Dihidrate)
onset gradual gradual acute
inflammation (-) (+) (+)
pathology degeneration pannus microtophi
Number of joints poly poly Mono to poly
Typical joint involvement Hips, knee, spine, 1st
CMC, DIP, PIP
MCP, PIP, wrist, feet,
ankles, knees
MTP, feet, ankle, knees
Joints often spared MCP, shoulder, elbow Lumbar and thorakal
spine, DIP
spine
Special articular findings Bouchard’s and
Heberden’s nodes
Ulnar dev, swan neck,
boutunniere deformities
Urate/CPPD crystal, tophi
Extra articular features SC nodules Olceranon bursitis, renal
stones
Lab data normal Often (+) RF ↑ UA (maybe normal
during flare)
5. OSTEOARTRITIS (OA)
Epidemiology :
• most common type of joint disease
• 80-90% individuals > 65 years have evidence of radiographic primary
osteoarthritis
• women > men
Pathology :
• degenerative disorder arising from the biochemical breakdown of articular
(hyaline) cartilage in the synovial joints
• pathophysiologic changes are also known to occur in the synovial fluid, as
well as in the underlying (subchondral) bone, the overlying joint capsule,
and other joint tissues.
6.
7.
8. Risk factors for osteoarthritis :
• Age
• Obesity
• Trauma
• Genetics (significant family history)
• Reduced levels of sex hormones
• Muscle weakness
• Repetitive use
Symptoms of osteoarthritis include the following:
• Deep, achy joint pain exacerbated by extensive use - The disease’s primary
symptom
• Reduced range of motion and crepitus - Frequently present
• Stiffness during rest (gelling) - May develop, with morning joint stiffness usually
lasting for less than 30 minutes
9. Diagnosis :
• Osteoarthritis is typically diagnosed on the basis of clinical and radiographic
evidence.No specific laboratory abnormalities are associated with osteoarthritis.
Treatment :
• Oral NSAIDs
• Topical NSAIDs
• Intra-articular corticosteroid injections
• Intra-articular sodium hyaluronate
• Muscle relaxants
• Nutraceuticals (eg, glucosamine/chondroitin sulfate)
• Lifestyle modification (exercise and weight reduction)
• Surgery (arthroplasty)
• Stem cell therapy
10.
11. GOUT & PseudoGout
• Gout and pseudogout are the 2 most common crystal-induced
arthropathies
• Gout is caused by monosodium urate monohydrate crystals;
pseudogout is caused by calcium pyrophosphate crystals à calcium
pyrophosphate disease (CPPD).
Epidemiology :
• Gout has a male predominance
• predominant age range of gout is 30-60 years
12. Pathophysiology :
• Gout can be considered a disorder of metabolism that allows uric acid or urate to
accumulate in blood and tissues
• Hyperuricemia may occur because of decreased excretion (underexcretors),
increased production (overproducers), or a combination of these two
mechanisms.
• When tissues become supersaturated, the urate salts precipitate, forming
crystals.
• the crystals also are less soluble under acid conditions and at low temperatures,
such as occur in cool, peripheral joints.
Clinical manifestation :
• Acute gout/ gout attack/gout flare
• Intercritical gout
• Chronic gout with tophi
13. Sign and Symptoms :
• Podagra (initial joint manifestation)
• Monoarticular involvement most commonly, though polyarticular acute flares are
not rare, and many different joints may be involved simultaneously
• attacks that begin abruptly and typically reach maximum intensity within 8-12
hours (at night or early in the morning)
• Without treatment, symptom patterns that change over time; attacks can
become more polyarticular, involve more proximal and upper-extremity joints,
occur more often, and last longer
• In some cases, eventual development of chronic polyarticular arthritis that can
resemble rheumatoid arthritis
• uric acid tophi (hard, uric acid deposits under the skin) contribute to bone and
cartilage destruction cause significant joint destruction and deformity
14. Diagnosis
• Joint aspiration à synovial fluid or tophaceous deposit analysis à
GOUT à needle-shaped negatively birefringent uric acid crystal
Pseudogout à rhomboid-shaped weak positively birefrigent crystal
• Serum uric acid measurement (though hyperuricemia is not
diagnostic of gout)
• Blood studies (including WBCs, triglyceride, high-density lipoprotein,
glucose, and renal and liver function tests)
• Plain radiographs (chronic gout à joints destruction)
• History of acute attack à intercritical phase without symptom
15. Treatment
Gout is managed in the following stages:
• Treating the acute attack
Ø NSAIDs, Colchicine, steroid oral/ intraarticular
• Providing prophylaxis to prevent acute flares (Lowering excess stores
of urate to prevent flares of gouty arthritis and to prevent tissue
deposition of urate crystals)
Ø Xantine oxidase inhibitor (allupurinol)
16.
17. SEPTIC ARTRITIS
• Septic arthritis, also known as infectious arthritis, may represent a direct invasion
of joint space by various microorganisms, most commonly caused by bacteria
(staphylococcus aureus, Neisseria gonorrhoeae)
• Organisms may invade the joint by direct inoculation, by contiguous spread from
infected periarticular tissue, or via the bloodstream (the most common route)
Pay attention to the following symptoms:
• Acuteness of onset of the joint pain (monoarticular)
• fever (40-60% of cases), pain (75% of cases), and impaired range of motion
• The presence of extra-articular symptoms
• Whether the patient has had vascular invasion due to catheterizations or
intravenous drug abuse
18. Work up
• Screen the synovial fluid for organisms via Gram stain
• An elevated erythrocyte sedimentation rate (ESR) or C-reactive
protein (CRP)
Treatment :
• Antibiotic (ceftriaxone, ciprofloxacin, dll)
• Synovial fluid drainage
• Joint immobilization and physical therapy
19.
20. Analysis of Joint Fluid
TEST NORMAL NON-
INFLAMMATOR
Y
INFLAMMATOR
Y
SEPTIC
appearance clear Clear, yellow Clear to
opaque (yellow
to white)
opaque
WBC/mm3 < 200 < 2000 > 2000 > 2000 (usually
> 50.000)
PMN 25% < 25% > 50% > 75%
culture (-) (-) (-) (+)
Intracellular
crystal
(-) (-) (+) in some (eg.
GOUT)
(-)
21. RA (RHEUMATOID ARTRITIS)
• Penyakit autoimun kronis progresif dengan manifestasi utama di
sendi. (poliartritis simetrik yang terutama mengenai sendi kecil
tangan dan kaki)
• Epidemiologi : wanita > pria
• Faktor resiko : usia lebih tua, jenis kelamin perempuan, riwayat
keturunan, riwayat merokok, dan paparan salisilat.
• Manifestasi klinis :
Ømanifestasi onset / awitan à gejala kronis gradual.
Ømanifestasi artikuler à kaku sendi > 1 jam, tanda tanda inflamasi, sinovitis,
deformitas sendi, poliartritis simetris
Ømanifestasi ekstrartikuler à nodul rheumatoid, vaskulitis, felthy sindrome, dll
22. 2010 ACR/EULAR CLASSIFICATION for RA SCORE
Joint involvement
1 large joint (ie, shoulders, elbows, hips, knees, ankles) 0
2-10 large joints 1
1-3 small joints (with or without involvement of large joints) 2
4-10 small joints (with or without involvement of large joints) 3
More than 10 joints (at least 1 small joint) 5
Serology test results
Negative rheumatoid factor (RF) and negative anti−citrullinated protein antibody (ACPA) 0
Low-positive RF or low-positive ACPA 2
High-positive RF or high-positive ACPA 3
Acute-phase reactant test results
Normal C-reactive protein (CRP) and normal erythrocyte sedimentation rate (ESR) 0
Abnormal CRP or abnormal ESR 1
Patient self-reporting of the duration of signs and symptoms
Shorter than 6 weeks 0
6 weeks or longer 1
23. EULAR RA management recommendations :
• Patients with active disease should be monitored every 3 months,
and treatment should be adjusted if there is no improvement at 6
months
• Methotrexate (MTX) is recommended as first-line therapy;
sulfasalazine (SSZ) or leflunomide can be substituted if there are
contraindications to MTX
• Tumor necrosis factor (TNF) inhibitors are no longer the only biologics
recommended for patients with an insufficient response to MTX; all
biologics are considered to be similarly effective
• Biologics should be combined with disease-modifying antirheumatic
drugs (DMARDs)
