Patho-4-OA Flashcards
What 5 changes would you expect to find in an osteoarthrtic synovial joint?
- irregular thickening & remodelling of sub-chondral bone with sclerosis & cysts
- thickening, distortion & fibrosis of capsule
- fibrillation, loss of volume & degradation of articular cartilage
- modest, patchy, chronic synovitis
- osteophytes & soft tissue growth at joint margin
T/F Most people >75 have OA changes in at least 1 joint
True
T/F: OA is more common in men than women
False
T/F Obesity does not correlate with OA
false - correlates best with knee OA
T/F OA is commonest form of arthritis
True
Prevalence of radiographic OA in men & women wrt joints commonly affected
Men - DIP > kneee - eak around 70
Women - DIP > knee > hip - peak around 70
Risk factors for OA
- trauma
- inflammatory arthritis, crystal arthropahy
- metabolic D/O (haemochromatosis, ochronosis)
- endocrine D/O (acromegaly)
- other bone & joint D/O (congential hip dysplasias, slipped capital femoral epiphyses, Paget’s, AVN)
Susceptibility - body bulid, hereditary, reproductive variables, osteoporosis, hypermobility, smoking, other diseases
Mechanical factors - trauma, joint shape, repetitive use (occupational, leisure)
What is OA?
- OA results from articular cartilage failure - complex interplay between genetics, metabolic, biochemical, biomechanical factors with secondary inflammation
- process - mismatched interaction between degradation & repair processes of cartilage, bone & synovium
- initiation process involves abnormalities in biomechanical forces &/or less often in cartilage
What is the hallmark feature of OA?
Degradation and loss of articular cartilage, with synovial inflammation
What cells are considered the most important for development of OA?
chondrocytes
Pathology of OA
- cartilage irregularity (fibrillation, clefts) –> ulceration of cartilage surface –> frank/rapid cartilage loss
- biochemically - reduced glycosaminoglycan content, increased water & increased MMP activity
Discuss early pathogenesis of OA
chrondrocytes exhibit transient proliferative response undergoing cloncal growth –> production of cytokines (TNF-alpha, IL1), growth factors, matrix-degrading enzymes
Major collagen type involved?
2
Discuss later pathogenesis of OA
initiating event attributed to mechanical stress –> altered chondrocyte metabolism & production of proteolytic enzymes & disruption of matrix properties
- first pathologic event may be multiple microfractures
What is arachindonic acid (AA)?
Omega 6 fatty acid precursor of pro-inflammatory prostaglandins and leukotrienes
What is the relationship between AA and OA?
Availability of AA for production of inflammatory eicosanoids could be a predisposing factor for synovitis
Why are omega 3 fats important?
- EPA and DHA are homologues of AA
- Makes for competitive inhibition of AA metabolism thus reducing inflammation, pain and synovitis
What joints is OA commonly found in?
- DIP
- PIP
- 1st CMC
- C & L spine
- 1st MTP of feet
- knee
- hip
Generalised OA?
3 or more joint groups involved/considered
What is generalised OA commonly associated with?
Herberden’s & Bouchard’s nodes
What joints are considered atypical for OA?
- MCPs
- wrist
- elbows
- shoulders
- ankles
Distribution of OA of hip joints x3
- Superolateral - most common (60%; M > F)
- Medial pole (25%, F > M)
- Concentric (15%, F > M)
Clinical Symptoms of OA
- Morning stiffness (Common <30mins)
- Worse in cold weather
- Insidious onset of pain (improves with rest or nocturnal pain in severe disease)
- Instability or buckling of joint (knee)
- growin pain, giat problems (hip)
- Problems with manual dexterity (CMC)
- nerve problems in lower C & L spine facet joints (osteophytes can narrow foramen & compress nerve roots)
Examination signs of OA
- Bony enlargement and bony tenderness at joints
- Jt instability
- Limited ROM
- Locking
- Crepitus
- Malalignment
- Pain in motion
- Joint effusion
- signs of inflammation in IP jts of hands with erosive OA
Radiographic features of OA
X-ray: - clinical dx confirmation
- osteophytes at margin
- assymetric jt space narrowing
- subchondral bone sclerosis
- subchondral cysts
Erosive OA - central erosions & cortical collapse in DIPs +/- PIPs of hands
Filli in this table
Goals of therapy for pts with OA
- control pain & sweling
- minimise disability
- improve QoL
- education on disease management
Examples of Non-pharm management
- Education
- Physio
- OT
- Social support
- Exercise
Examples of Pharm management
- Topical - capsaicin
- Oral - non-opioid analgesics (paracetamol, tramadol), NSAIDs/COX2 inhibitors, opiods, glucosamine & chrondoitin, fish oil
- Systemic
- Intra-articular (Corticosteroids)
Using a table discuss clinical difference between RA and OA in terms of primary joints affected, Heberden’s nodes, joint characteristics, stiffness, lab findings
