Rheum - Reactive Arthritis Flashcards
Define Reactive Arthritis
STERILE inflammation in joints FOLLOWING infection especially
• urogenital (e.g. Chlamydia) & gastrointestinal (e.g. Salmonella, Shigella) infections
Key points associated with Reactive Arthritis?
Important extra-articular manifestations include:
• Enthesopathy – a disorder relating to the ligament attaching to the bone
• Skin inflammation
• Eye inflammation
ReA may be the first manifestation of HIV or Hep C infection
Commonly affects young adults (with a genetic disposition – e.g. HLA-B27) with an environmental trigger such as a Salmonella infection
Symptoms follow 1-4 weeks after infection (may be mild)
ReA is distinct (sterile) from infection in the joints
• known as SEPTIC arthritis.
Is there a biomedical test to check for ReA?
NO as it is ‘seronegative’
Musculoskeletal symptoms of ReA?
Arthritis:
Asymmetrical
Oligoarthritis – less than 5 joints affected
Lower limbs more affected
Enthesitis:
Heel pain – Achilles tendonitis
Swollen fingers – dactylitis
Painful feet – metatarsalgia due to plantar fasciitis
Spondylitis:
Sacroiliitis – inflammation of the sacro-iliac joint
Spondylitis – inflammation of the spine
Extra-articular features of ReA?
Ocular:
Sterile conjunctivitis
Genito-urinary:
Sterile urethritis
Skin:
Circinate balanitis
Keratoderma blennorrhagicum
What was the original description of ReA?
arthritis, urethritis and conjunctivitis following infectious dysentery (Reiter’s syndrome)
Compare RA vs. ReA
Onenote!!
Sex Ratio Age Arthritis Enthesopathy Spondylitis Urethritis Skin involvement Rheumatoid factor HLA association
Compare Spetic A vs. ReA?
Onenote!!
Synovial fluid culture
Antibiotic therapy
Joint Lavage
What is one of the biggest things about RA in the comparison table
Note how RA affects the ATLANTO-AXIAL JOINT (
• as this spinal joint contains synovial fluid
How is diagnosis achieved for ReA?
3 main ways:
Clinical diagnosis – i.e. asymmetrical arthritis
Investigations of exclusion – i.e. septic arthritis
Other investigations:
• Microbiology:
- Microbial cultures – stool, blood, etc.
- Serology – e.g. HIV, Hep C.
• Immunology:
- RF.
- HLA-B27.
• Synovial fluid examination – only if a single joint is affected.
How is ReA treated?
In majority, resolution in 2-6months
NO ROLE for antibiotics
Articular:
• NSAIDs
• Intra-articular corticosteroid therapy
Extra-articular:
• Symptomatic therapy – topical steroids
Refractory disease – non-responsive to treatment:
• Oral glucocorticoids
• Steroid-sparing agents – DMARDs
Define Osteoarthritis
Chronic, slowly progressive disorder due to failure of articular cartilage, typically affecting joints of the • hand • spine and • weight-bearing joints
What joints does osteoarthritis normally affect?
Joints of the hand
• DIP, PIP, CMC (1st carpometacarpal joint)
• NOT MCP
- Herberden’s nodes - osteophytes at DIP joints
- Bouchard’s nodes – osteophytes at PIP joints
Before (proximal) = Bouchard
Spine
Weight-bearing joints of the lower limbs
• hip/knee, MTP (1st metatarsophalangeal joint)
What is osteoarthritis associated with?
o Joint pain
• worse with activity
o Joint crepitus
• creaking sound on movement
o Joint instability
o Joint enlargement
• i.e. Herberden’s nodes.
o Joint stiffness after immobility and limitation of motion.
What are radiographic features of osteoarthritis?
o Joint space narrowing
o Subchondral bony sclerosis
• hardening of the bone on the subchondral portion
o Osteophytes
• new bony formations (at joint margins)
o Subchondral cysts
Radiographic changes in RA vs. OA?
Onenote!!
Joint space narrowing
• occurs in BOTH due to different reasons
• cartilaginous loss in RA is caused by 2o damage due to synovitis vs. in OA where is it the 1o abnormality
Subchondral sclerosis
Osteophytes
Osteopenia
Bony erosions
Pathogenesis of OA?
There is defective and irreversible articular cartilage and damage to the underlying bone
This develops due to (and/or):
• Excessive loading on joints – more apparent in the old
• Abnormal joint components – more apparent in the young
What is the most important component of the articular cartilage?
AGGRECAN!
The weight-bearing properties of the articular cartilage depend upon the
• intact collagen scaffold & the high aggrecan content
Aggrecan is made up of
• Chondroitin sulphate & Keratan sulphate
• The GAG chains are important at absorbing water to be used to resist compressive forces.
Explain ECM proteoglycans
Proteoglycan – glycoproteins containing 1+ sulphated glycosaminoglycans (GAG) chains
GAGs are repeating polymers of disaccharides and include: Chondroitin sulphate. Heparan sulphate. Keratan sulphate. Dermatan sulphate. Heparin.
Examples:
Intra-cellular – Serglycin.
Cell-surface associated – Betaglycan, Syndecan.
Secreted into ECM – Aggrecan, Decorin, Fibromodulin, Lumican, Biglycan.
What in unique about Hyaluronic acid?
Is the ONLY non-sulphated GAG
• and has an important role in maintaining synovial fluid viscosity
What is the major proteoglycan in articular cartilage?
Aggrecan
Explain the cartilage changes in OA
Reduced proteoglycan
Reduced collagen
Chondrocyte changes
• e.g. apoptosis
Explain the bone changes in OA
Changes in sub-articular bone:
• Proliferation of superficial osteoblasts resulting in sclerotic bone
• Focal stress on sclerotic bone focal superficial necrosis
New bone formation at joint margins (bone spurs):
• Examination can detect these.
• Herberden’s nodes vs Bouchard’s nodes.
Management of OA?
o Education.
o Physical therapy.
o Occupational therapy.
o Weight loss (where appropriate) and exercise.
o Analgesia – paracetamol, NSAIDs, intra-articular corticosteroid injections.
o Joint replacements.
Provided the joint is functional, all you have to do is CONTROL the PAIN
• strengthening the muscle around the joint will improve mechanical stability of the joint
