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