Joints History Flashcards
How would you differentiate between inflammatory and non inflammatory causes of joint pain?
Inflammatory
- systemic symptoms, v prominent fatigue
- insidious onset (seropositive, seronegative)
- sudden onset (infection, gout)
- morning stiffness, 1hr+
- worst pain on waking and when resting
- pain decreases with activity but increases with overuse
Non inflammatory
- unusual to have systemic symptoms
- gradual onset (mono/oligoarthritis)
- morning stiffness, U1hour
- pain increases as day progresses, worsens with activity
- pain improves with rest
What is the
- pathophysiology
- signs
- investigations for RA
HLA DR1-4 genetic predisposition to present citrullinated self proteins on surface => recognised as foreign by adaptive immune system
Release of pro inflammatory cytokines leads to
-osteoclast activation
-synovial membrane thickening, angiogenesis
-protease, collagenase production => bone and cartilage erosion
Signs
- tenderness and swelling
- hot
Early
- symmetrical swollen MCP, MTP, PIP, wrist joints
- tenosynovitis, bursitis
- spongy on palpation
Late
- ulnar deviated fingers
- hitchhiker thumbs, swan and Boutonnière fingers
- rheumatoid nodules
Medical history
-CVD, ILD
Investigation findings
- Anaemia of chronic disease
- RF, anti CCP
- raised CRP, ESR
- low albumin (leakage of protein into tissue due to inflammation)
What are the findings of RA on X-rays
Loss of joint space
Erosion of bone and cartilage
Soft tissue swelling
Soft bones (osteopenia)
How would you treat RA
- flare up
- maintenance of remission
Use DAS28 to judge remission or flare up
Flare up
-short term NSAIDS, CS
Long term (DMARDs) -methotrexate/HCQ/sulfasalazine
Long term (biologics)
- TNFa - adalimumab, influximab, etanercept
- IL1 - anakinra
- IL6 - toclizumab
- Bcell suppression - rituximab
- Tcell suppression - abatacept
What is the
- pathophysiology
- signs
- investigations for OA
Wear and tear of joints => loss of articular cartilage => bone ends rub together
Increased predisposition
-genetics, female
-biomechanical stress and loads
Signs
- Asymmetrical swelling and tenderness of DIP, thumb bases
- Bony overgrowths with crepitus
- Heberdens, Bouchards nodes
- Effusions, cool
- Pain on passive, active movement with limitations
Investigations
- FBC => no anemia of chronic disease, no infection
- normal CRP, ESR
- no RF, CCP
What are the X-ray findings of OA
Loss of joint space
Osteophytes
Subchondral cysts
Sclerosis (whitening of bone)
How would you manage OA
Lifestyle changes
-exercise, physiotherapy
Topical analgesia -capsaicin or NSAIDS May add -paracetamol -NSAIDS/capsaicin -codeine/oxycodone/tramadol
DON’T FORGET PPI for NSAID gastroprotection
Last line => joint replacement surgery
What is the
- pathophysiology
- signs
- investigations for septic arthritis
Signs
- sudden red hot swollen single joint after haematogenous spread/direct inoculation with underlying infection
- tender to touch, limited movement
- effusion, pain on active movement
- systematic symptoms
Investigation
- FBC, blood cultures => signs of infection
- high CRP
- U&E => impact on kidneys
- Joint aspiration => gram staining, microbiology, WCC, culture
How would you manage a potential case of septic arthritis
-what are the likely causative organisms
Staph aureus = most common
N gonococcus = sexually active
EColi = UTI
Suspected infection => broad spec empirical ABx
-once causative organism identified (most likely staph aureus) => narrow spec
If needed, surgical irrigation and debridement for source control
What is the
- pathophysiology
- signs
- investigations for gout
Inflammatory crystal monoarthropathy caused by monosodium urate crystals in big toe
Signs
Rapid onset
Heat, pain, redness, swelling in big toe/knee
Tophi on tendon surfaces
Symptoms of renal calculi
Systemic symptoms like with septic arthritis
Investigations => RULE OUT SEPTIC ARTHRITIS FIRST
- FBC => leukocytosis
- high CRP, ESR
- U&E => assess for any kidney damage from renal stone
- synovial fluid aspiration => needle shaped negative birefringent monosodium urate crystals
What are the risk factors for gout
Genetics, age, male, post menopausal Overweight Purine rich diet -red meat, sea food, alcohol Thiazides, ACEi
Cytotoxic => tumour lysis
How would you manage gout
- flares
- remission
- lifestyle
Flares - 1st line -NSAIDs (avoid aspirin) or CS (PPI for gastroprotection) -Colchicine 2nd line -IL 1 - anankira, canakinumab
Ongoing
-allopurinol or febuxostat or sulfinpyrazone => urate lowering agent
Lifestyle
- reduce alcohol, low purine diet
- stop/swap thiazides, ACEi (CCB can be protective)
What is the
- pathophysiology
- signs
- investigations in pseudogout
Inflammatory crystal monoarthropathy caused by deposition of calcium pyrophosphate crystals in the knee/wrist/larger joints shed from cartilage
Similar to septic arthritis
- heat, pain, red, swelling
- larger joints, elbow, wrist, ankle
- joint effusion
Investigations
- FBC => leukocytosis
- high CRP, ESR
- U&E => assess for any kidney damage to rule out gout
- synovial fluid aspiration => positively birefringent rhomboid crystals under polarised light
What are the risk factors for pseudogout
Older age, genetics
Joint trauma
Excess Ca, not enough Mg
Hypothyroidism, hyperparathyroidism
How would you manage pseudogout
- acute (monoarticular/polyarticular)
- maintenance
- lifestyle
Aim to reduce pain and improve function of joints
Acute mono/oligoarticular
- CS injections and paracetamol for pain
- if not possible => NSAIDs and colchicine (1st line for polyarticular)
- delay use of systemic CS
Chronic
-joint replacement surgery
Lifestyle
-cool packs, rest, aspiration
