Rheumatology - ix Flashcards
OA ix
XRAY LOSS
• Loss of joint space/ Non-uniform joint space narrowing
• Osteophytes
• Subchondral sclerosis/Subchondral bony sclerosis
• Subchondral cysts/Bone cysts
• Joint aspirate
Straw coloured fluid
Increased viscosity
• Normal blood tests
RA ix
Bloods
• Rheumatoid factor
IgM antibody that targets other IgG antibodies
Most sensitive
• Anti-cyclic citrullinated peptide antibodies (anti CCP)
Most specific
• ACD, increased ESR/CRP, low albumin
Radiology (first one most common, then decreasing order)
- uniform joint space narrowing
- soft tissue swelling
- juxta-articular erosions
- joint subluxation
- osteopenia
- Joint erosions at joint margins
- joint deformity + destruction
Amyoidosis ix
• Tissue biopsy
o Congo red stain – pink in real life, apple-green birefringence when viewed under polarised light
• Immuo-electro microscopy
o Amyloids - Fibrillar, rigid, non-branching
• Mass spectrometry
o Gold standard for amyloid typing
o Provides analysis of amyloid protein composition
• 24h urine collection
o >1g/24h urinary albumin - renal involvement in amyloidosis
o >3g/24h urinary albumin - nephrotic syndrome
- Increased ESR, N CRP
- Blood film - Howell Jolly bodies
- Hepatic amyloidosis - low albumin, increased ALP
- Renal amyloidosis - low albumin, N creatinine
AL amyloidosis (primary) - caused by plasma cell disorders • Serum immunofixation + Urine immunofixation o Presence of monoclonal protein (in immunoglobulin light chain amyloidosis)
• Immunoglobulin free light chain assay
o Abnormal kappa to lambda ratio
• Bone marrow biopsy
o Clonal plasma cells (gamma > kappa)
The finding of light chain protein in the urine is suggestive of multiple myeloma + amyloidosis (have in mind that amyloidosis is caused by multiple myeloma)
Ankylosing spondyltis ix
• Pelvic XR
o Sacroiliitis
o A dx of established AS requires definitive evidence of sacroiliitis on XR
• Cervical spine, thoracic spine, lumbar spine XR
o Erosion
o Joint space narrowing
o Squaring sclerosis
o Syndesmophyes
o Ossification of spinal ligaments
o Bamboo spine (complete fusion of the vertebral column)
o Romanus lesions - erosion of the corners of the vertebral bodies
• MRI
o Useful in identifying early sacroiliitis before XR changes are apparent
o XR changes take may years to develop and represent established damage
- HLA-B27 – not diagnostic, genetic testing to help confirm the dx
- US – to confirm/quantify the extent of enthesis
• Schober’s test
o Patient in a standing position
o Mark L5
o Then mark 5 cm below and 10 cm above L5 (total distance of 15 cm)
o Ask patient to touch his/her toes while keeping the knees straight
o Distance of the two points must increase by at least 5 cm (with the total distance greater than 20 cm)
o If not –> restricted lumbar flexion
Bloods may show - ACD, raised ESR, CRP
Diagnostic criteria for anlylosing spondylitis (modified New York criteria)
Definite AS – radiological criterion + at least 1 clinical criterion
Probable AS – 3 clinical criteria // radiological criterion w no clinical criteria
Clinical criteria
• Low back pain >3 months [Improved by exercise, not relieved by rest]
• Limitation of lumbar spine motion in both sagittal + frontal planes
• Limitation of chest expansion relative to normal values for age + sex
Radiological criterion
• Sacroiliitis on X-ray
Reactive arthritis ix
Bloods
• HLA B-27
• ESR + CRP high
• Normocytic anaemia, mild leucocytosis, thrombocytosis
• Synovial fluid examination
WCC
Required to rule out septic/crystalline arthritis
Septic arthritis ix
• Joint aspirate o Before abx o Turbid yellow o Low viscosity o Increased WCC (neutrophils >90%)
- MCS of joint aspirate
- XR – Joint space narrowing due to cartilage destruction
- US – can detect early effusions + guide joint aspiration
- CT+ MRI – periarticular abscesses, joint effusions, osteomyelitis
- Bloods - Increased WCC, CRP
Gout ix
• increased serum urate levels
Should be obtained at least 2 weeks after the attack resolves as it may be falsely low or normal during the attack
• Synovial fluid analysis + Electron microscopy
o Monosodium urate crystals in or outside the cell
o Sharp, needle-like form
o Negatively birefringent under polarised light (yellow under parallel light, blue under perpendicular light)
o Raised WBC count with neutrophil dominance
o Low viscosity
• Gram stain + culture – to exclude infection
• XR or CT for chronic gout
o Crystal deposits
o Periarticular erosions ("rat-bite" erosions)
sclerotic margins
overhanging edges
o Punched out periarticular erosions
• Bloods
o Raised WCC (neutrophil dominance)
o Raised CRP
o Uric acid after 4-6 weeks
Pseudogout ix
• Synovial fluid analysis + Electron microscopy
o Calcium pyrophosphate crystals in or outside the cell
o Rhomboid or rod-shaped appearance
o Weakly positively birefringent under polarised light (blue under parallel light, yellow under perpendicular light)
o Raised WBC count with neutrophil dominance
o Low viscosity
• Imaging
o Chondrocalcinosis – cartilage calcification
• Screening for
o Hyperparathyroidism (serum calcium, serum PTH)
o Hypothyroidism
o Hypomagnesemia (serum magnesium)
o Hypophosphatasia (serum ALP)
o Hemochromatosis (iron studies – serum ferritin, iron, TIBC)
• Bloods
o Raised WCC (neutrophil dominance)
o Raised CRP
Osteomyelitis ix
Bloods
• FBC - WBC
• raised ESR, raised CRP
• Blood cultures
Imaging
1st line • XR - May be helpful in dx of chronic osteomyelitis
o Thickening of the cortical bone + periosteum
o Elevation of the periosteum (Periosteum loosely attached to cancellous bone - two layers can separate - abscess can form between them)
o Loss of the normal architecture of the bone (especially trabecular architecture)
o Osteopenia
o Evidence of bone destruction
2nd line (under ix to consider) • Bone scan/MRI
o Imaging modality of choice for ix of acute osteomyelitis (most sensitive)
o Confirm the presence of osteomyelitis
- Bone deformity
- New bone formation from the cortex outwards
- Gas in soft tissues
- Reduced opacity
o Identify an abscess
• US
o Useful in acute osteomyelitis
o Look for signs of associated septic arthritis + infection
o May show collections, subperiosteal abscesses, adjacent joint infusions
o Helpful in guiding aspiration or biopsy for microbiological dx
• CT scan
o Useful for visualising extent of bone destruction
• Bone biopsy
o Culture + identify pathogen responsible
o Confirm dx
• PET scan
o Increased uptake of radioactive injectate in infected sites
o To differentiate between active infection and structural derangement of the bone
Idiopathic inflamatory myopathy
• Raised CK
• EMG
o Dead muscle cells –> abnormal electrical signal conduction + evidence of muscle membrane irritability
o Short duration, low amplitude, polyphasic units with early recruitment on voluntary activity
• Muscle biopsy to confirm dx
o Polymyositis - CD8+ T lymphocyte infiltrate the endomysium, muscle necrosis, atrophy
o Dermatomyositis - CD4+ T lymphocytes infiltrate the perimysium, perifascicular atrophy
o Inclusion body myositis β-amyloid plaques collect within muscle fibres (can be revealed by Congo red staining)
• Increase in muscle enzymes CK LDH aldolase Less specific than CK for monitoring activity Present in muscle + liver AST, ALT Less specific for muscle injury than CK myoglobin
• +ve ANA (in dermatomyositis + polymyositis)
• Myositis specific autoantibodies
o Polymyositis (anti-cytoplasmic antibodies against translational components)
Anti-Jo12
Anti- SPR
o Dermatomyositis
Anti-M2
Anti-mas
• ESR + CRP
• Increase Soluble CD30
o Expressed mainly by activated CD+ T cells
o Increase in polymyositis + dermatomyositis
• FBC – ACD (microcytic)
• MRI
o Large areas of inflammation, oedema, fibrosis, calcification
• US
o Image suggestive of inflammatory processes
To diagnose - CK + EMG
To confirm dx - muscle biopsy
Diagnosis of idiopathic inflammatory myopathy
Diagnosis of polymyositis (first four criteria must be met) + dermatomyositis (3 out of the first four + the 5th criteria must be met)
- Bilateral proximal myopathy – involving both thighs or both upper arms
- Increased muscle enzymes
- Abnormal electrical signal conduction on electromyography
- Lymphocyte infiltration + abnormal muscle degeneration on biopsy
- Presence of skin rashes
Sarcoidosis ix
• CXR
o Bilateral hilar lymphadenopathy (+/- hilar infiltrates)
o Pulmonary infiltration/fibrosis
• Raised serum calcium, raised urine calcium
o Due to dysregulated production of calcitriol by activated macrophages + granulomas
• Raised serum ACE (from T-cells)
• Raised ESR
• Biopsy (flexible bronchoscopy with transbronchial lung biopsy)
o Essential for dx
o Non-caseating granulomas
o Langhans giant cell
• FBC
o Anaemia
o Leukopenia/leucocytosis/eosinophilia
o Secondary to BM involvement
• BAL
o Lymphocytosis
o CD4-to-CD8 ratio >3.5
• PFTs
o To monitor disease
o Persistent decline in FVC indicates disease progression
o Restrictive/obstructive/mixed pattern
SLE ix
- FBC – normocytic normochromic anaemia, leukopenia, thrombocytopenia
- ESR + CRP – elevated
- ANA – most sensitive but NON-diagnostic as it’s very non-specific
- Anti-ds-DNA antibody – highly specific for SLE, confirmatory of the dx, level reflects disease activity
- Anti-cardiolipin ab
- Anti-Smith antibody – highly specific for SLE, confirmatory of the dx, ab against small ribonucleoproteins
- U+E - raised U + Cr if pt w SLE have renal manifestations
- Urinalysis – to assess renal involvement (haematuria, casts, proteinuria)
- (Biopsy of the kidney – diffuse thickening of the glomerular capillary walls with “wire loop” structures) –might be in an SBA
- Skin biopsy – only done when dx is in doubt, immune deposits at the dermal-epidermal junction on immunofluorescence, non-specific inflammation
- Low complement levels – Complement C3 + C4 levels are decreased
APLS –> complication of SLE (thromboembolism, miscarriage, thrombocytopenia)
• Antiphospholipid antibodies – anticardiolipin, anti-b2-glycoprotein I, lupus anticoagulant – checked in lupus patients as APLS can occur secondary to autoimmune diseases like SLE
• APTT – may be prolonged in patients with antiphospholipid antibodies
Positive ANA anti-histone antibodies with negative anti-dsDNA antibodies
drug-induced lupus erythematosus
o Develops as a reaction to certain medication metabolised by N-acetylation in the liver
o Does ont affect the oral mucosa, CNS or kidneys
o SHIPP – sulphonamide, hydralazine, isoniazid, procainamide, phenytoin
