Deck 10 Flashcards
Infective joint pain
Rubella, parvovirus, mumps, Hep B, staphylococci, TB, borrelia
Post infective joint pain
rheumatic fever, reactive arthritis
Inflammatory causes of joint pain
RA, ankylosing spondylitis, SLE, scleroderma, polymyositis
Tumour joint pain causes
primary (osteosarcoma, chondrosarcoma)
Secondary (lung, breast, prostate)
Joint pain with hypermobility
Ehler’s danlos
OA most common joints
knee (often bilateral), hip and small hand joints (DIPS)
Metatarsophalangeal joint, talonavicular joinr, lumbar and cervical spine
crystal associated OA
chondrocalcinosis (calcium pyrophosphate crystals - knees and wrists).
OA S+S
Pain worse on movement, morning stiffness <30 mins
Heberdens nodes, bouchards nodes, thumb squaring, varus knees (medial tibiofemoral OA),
Osteophytes, reduced range of active/passive movement, crepitus, deformity, effusion, atalgic gate
OA RF
genetic (esp hands), aging, female, obesity, high bone density, Hx of joint injury, occupation, reduced muscle strenth, joint malalignment
Typically W>M, 50_
Secondary OA
crystal arthritis, avascular necrosis, acromegaly, haemochromatosis, chondrocalcinosis, haemophilia, haemoblobinopathies, neuropathies
OA definition
clinical outcome of various factors giving pain, disability, stricutral synovial joint failure and remodelling
OA diagnosis
Xray scoring, but not needed for diagnosis. Loss of joint space Osteophytes Subchondral sclerosis Subchondral cysts Cartilage degradation
Hip has painful and reduced rotation, and positive trendelenburg test (sound side sags)
RA
Symmetrical inflammatory polyarthropathy
RA pathophysiology
Neutrophil /T cells, macrophages infiltration during rheumatoid synovitis, exudative effusion, then vascular granulation (pannus via osteoclast and macrophages causes erosions)
Can be secondary to OA
Morning stiffness can be inflammatory mediators or excess cortisol
RA S+S
fatigue, sleep impacted. flares (can be med change, stress, poor adherence - may trigger med review), pain, swelling, erythema in small joints of hands/feet (bilateral)
MCP, PIPs, wrist, elbow, glenohumeral, cervical spine, hip, knee, ankle.
Thoracic/lumbar spine and dips are spared
Morning stiffness lasts >30 mins.
Often goes from feet to hands to knee to shoulder/hip
Valgus deformity and secondary OA can develop
Advanced RA
Ulnar MCP, radial wrist, boutoniere (dip flex, pip extend) or swan neck (pip and dip extension), Z thumb (IP extension, flexed MCP)
Joints sublux, deformity occurs with ankylosis
Pannus formation
vascularised granulation tissue. Synovial membrane becomes hypertrophied
Skin RA features
nodules (esp in seropositive RA), fragility, vasculitis, pyoderma gangrenosum
Heart RA features
pericarditis, atherosclerosis, vasculitis, valvular disease
Lung RA features
pleural effusion, fibrosis, bronchiolitis obliterans (dry cough, SOB), RA nodules, vasculitis
Eye RA features
keratoconjunctivitis sicca (sjogrens), episcleritis, scleromalacia perforans (necrotising scleritis), peripheral ulcerative kerotopathy
Neurological Ra features
carpal tunnel, peripheral neuropathy
Haematopoeitic Ra featuures
anaemia, thrombocytosis, lymphadenopathy, felty syndrome
Felty syndrome
RA , splenomegaly, neutropoenia
Kidney RA features
amyloidosis, vasculitis
Bone RA features
osteopoenis
Nodules in RA form
Local vascular damage allows IgM rheumatoid factor complex to embed in vessel walls. Stimulates monocytes and leads to pallisading granuloma formation
palisading granuloma
macrophages and giant cells in tier formation
RA diagnosis
anti CCP is most specific
RF also used, but can be FP as not as specific
ANA raised if CT disease
XR shows loss of joint space, erosions
Normocytic anaemia of chronic disease, leukocytosis, raised CRP/ESR
Non joint complications of RA
GI bleed due to aspirin therapy, infections/osteoporosis due to steroids, amyloidosis
DDx in early RA
reactive arthritis, seronegative spondyloarthropathies, polymyalgia rheumatica, acute nodal OA
Gout investigations
FBC, CRP, ESR, serum urate, synovial fluid aspiration, HbA1c, lipid profile
xray (punched out erosions)
Gout diagnostic test for crystals
negatively birefringent needle - > urate
Primary gout
Either excess uric acid production or reduced excretion. Alcohol and obesity predispose
Secondary gout
10% of cases. Associated with increased nucleic acid turnover
- diuretics, aspirin, nicotinic acid, lead, glycogen storage disease
Pathophysiology of gout
Typically monoarticular
Crystals activate Hageman factor (inflammation and chemo attractant -macrophages/neutrophils phagocytose crystals and secrete lysozymes, PGs etc which inflame and cause synovitis)
Renal effects of gout
tophi, intratubular urate deposition, nephrolithiasis, chronic urate nephropathy
Pseudogout associated conditions
Typically elderly patients
Associated with hyperparathyroidism, hypophosphataemia, hypomagnesaemia, Wilson’s disease. But may be sporadic
Typical pseudogout joints
often knee, but can get wrist
Pseudogout investigations
Chondrocalcinosis (calcification of articular cartilage and menisci on xray)
Weakly positive,blunted rhomboid calcium pyrophosphate dihydrate crystals)
Most common septic arthritis in children
H influenzae
Most common septic arthritis in older childrenadults
Staphylococcus aureus
Pott disease
Spinal TB
TB arthritis
insidious, chronic onset. Often haematogenous spread, or from osteomyelitis focus.
Lyme disease arthritis
Post skin signs. Migrates. Involves large joints. Often clears spontaneously but may cause long term damage