MSK CBL Flashcards
Cardinal features of OA
Pain aggrevated by movement and relieved by rest
Pain aching in character and poorly localised
Muscle spasms around the joint
Stiffness waking in the morning
Joint deformity and wasting of associated muscles
Joint swelling
Localised tenderness
Palpable ostephytes and crepitus
Limp or antalgic gate
Tests to confirm OA
X ray and blood tests
What would x-ray show in OA?
Loss of joint space
Subchondral sclerosis
Bone cysts
Osteophytes at lateral margin of joint
Which blood tests would be done in OA and what would the results be?
FBC - normal
ESR, CRP - normal
RF, anti-nuclear factor - negative
Calcium,phosphate, alkaline phosphatase - normal
Secondary OA abnormalities may include - high levels uric acid (gout) or alkaline phosphatase (pagets)
Mx of OA
Pain relief - analgesics and anti-inflammatories
Increase mobilisation - phsyio
Reduce load - weight loss, walking stick
Surgical - osteotomy, arthrodesis, joint replacement
Osteotomy
Can relieve pain - may change mechanical axis of joint to allow weight bearing on the part of the articular surface which isn’t affected
Arthrodesis
Best performed when adjacent joints are relatively unaffected. May be considered in young px whom a joint replacement may fail.
Joint replacement
Remains best tx for OA of hip and knee
6 features of a synovial joint
Smooth articular cartilage at bone ends
Joints surrounded by connective tissue capsule
Joint cavity
Synovial membrane
Capsule reinforced by ligaments
Joint capable of movement
Macroscopical pathological features in OA
Subarticular cysts
Osteophytes at joint margin
Sclerosis of subchondral bone
Loss of articular cartilage with eburnation of surface
Microscopical pathological features in OA
Fissuring, flaking then full thickness loss of articular cartilage
subarticular cysts
osteophytes at joint margin
sclerosis of subchondral bone
OA cartilage
Increased water content, alterations in proteoglycans, collagen abnormalities, binding of proteins to hyaluronic acid
Changes in synovium in OA
Detritus synovitis - flakes of bone and cartilage broken off from damaged joint embed in synovium = mild villous hyperplasia and chronic inflammation
Causes of OA
Primary OA
Secondary OA - high intensity impact, previous joint sepsis, charcot’s joint, paget’s disease, avascular necrosis
Inv for RA
Haematology - FBC Blood film Haematinics LFT's
Immunology - Autoantibodies (ANA, RF, complement) Immunoglobulins Serum protein electrophoresis CRP
What results would be expected from blood tests in RA?
FBC - low haem, elevated ESR
Blood film - anaemia of chronic disease
Haematinics - depends on form of anaemia
LFTS - normal, mildly elevated alkaline phosphatase and maybe gamma GT
Results expected from immunology in RA?
Autoantibodies -
ANA - negative
RF - positive
Complement - normal
Immunoglobulins -
Increase IgG and IgA, normal IgM
CRP high
Anti CCP antibodies
X ray changes in RA
Periarticular osteopenia
Periarticular erosions
soft tissue swelling around metacarpo-pharyngeal joints
Histological changes in RA
Villous architecture abnormalities Synovial lining hyperplasia Fibrin exudation Chronic inflammation with lymphoid aggregates and plasma cells Pannus destroying cartilage
Pathogenesis of RA
Joint swelling due to active synovities
Synovium full of macrophages, T lymphocytes and plasma cells (producing RF)
Macrophages activated - proinflamm cytokines e.g. TNF, IL-1 and IL-6 activate enzymes
Pannus forms and destroys cartilage and bone
Which other systems can be affected by RA?
CVS - pericarditis, myocarditis, vasculitis
Resp - pleuritis, pulmonary fibrosis
Haem - anaemia, splenomegaly
RA mx
NSAIDs
DMARDS - methotrexate
Corticosteroids - intra-articular, IM or oral often used until DMARDs take effect
Biological - anti TNF (infliximab), rituximab, tociluzimab
Surgical interventions for RA
Tendon repair
Synovectomy
Joint replacement
Joint fusion
