Rheumatology Flashcards
What medications are effective for osteoarthritis?
NSAIDs
Duloxetine (SNRI)
Intra-articular glucocorticoids
What is fibromyalgia and its clinical features?
Central nociplastic pain disorder
Chronic widespread pain
Allodynia
Fatigue
Fibrofog
Sleep disturbance
Mood disturbance
Sensory sensitivity
Medication intolerance
Altered interoception
How is fibromyalgia managed non-pharmacologically?
Movement practice (exercise)
Attention to sleep
Cognitive therapy
What medications can be used in the management of fibromyalgia?
TCAs
Gabapentinoids
SNRIs
Tramadol
How is rotator cuff disease diagnosed?
Clinically, no role for imaging
How is rotator cuff disease managed?
Non-invasively with time, PT and NSAIDs
How is greater tronchateric pain diagnosed?
Clinically, features of maximal tenderness over greater trochanter, positive Trendelenberg test
How is greater trochanter pain managed?
PT and analgesia
No evidence to support gluco-corticoid injection
What conditions are associated with yellow nail syndrome? How is it managed?
Chronic resp illness, lymphoedema, rarely RA, malignancy, immunodeficiency
Treatment includes Vit E, zinc, itraconazole (speeds up nail growth not antifungal activity)
What is the classical appearance of mycosis fungiodes?
Poikilodermatous patches= (hypopigmentation, hyperpigmentation, telangiectasias and atrophy) in bathing suit distribution
What are histological features of neutrophilic dermatoses?
Diffuse neutrophilic infiltrates in absence of identifiable infection
What are clinical feature of Sweet Syndrome (acute febrile neutrophilic dermatosis) and how is it treated?
Fevers, infiltrated plaques +/- bullae on head and neck
Associated with AML, IBD
Treated with high dose oral prednisolone and treatment of underlying condition
What is the treatment for vitiligo?
Topical steroids or tacrolimus
What HLA types are associated with DRESS to anti-retrovirals?
HLA-B5701 and abacavir
HLA-B3505 and nevirapine
How is lipoatrophy associated with anti-retrovirals for HIV treated?
Switching to non-thymidine agents (didanosine, lamivudine, zalcitabine)
Pravastatin
What medications are commonly associated with SJS and TENS?
Allopurinol, NSAIDs, antibiotics, anti convulsants
What is the key difference between SJS and TENS?
BSA involved
< 10% = SJS
> 10% = TENS
What HLA type is associated with SJS/TEN and carbamazepine?
HLA-B*1502, Han Chinese esp in Taiwan
How is SJS/TEN managed?
Admission to ICU or Burns unit
Fluids
DVT prophylaxis
IVIg 1g/kg/day for 3 days
What immunological tests are associated with dermatomyositis?
ANA, anti-Jo1, anti-p55/140 (cancer), anti-Mi2
What are the two types of axial apodyloarthritides?
- Axial spondyloarthritis: involves spin and sacroiliac joints
- Peripheral spondyloarthritis: involve peripheral joints or entheses or dactylitis
How is axial spondyloarthrtitis classified?
3 months of inflammatory back pain and age of onset < 45
AND
Sacroilitis on imaging + 1 feature of axial spondyloarthrtitis
OR
HLA-B27 positive and 2 other features of axial spondyloarthrtitis
What are clinical features of axial spondyloarthrtitis?
-inflammatory back pain
- arhtritis
- enthesitis
- uveitis
- dactylitis
- psoriasis
- crohn’s/colitis
- good response to NSAIDs
- family history of SpA
- HLA-B27
- raised CRP
What is the diagnostic criteria for peripheral apondyloarthritis?
Peripheral arthritis and/or enthesitis and/or dactylitis
AND
1 non-joint SpA feature
OR 2 other joint SpA features
What is inflammatory back pain?
- age onset < 40
- insidious onset
- improves with exercise
- no improvement with rest
- pain at night (2nd half of night)
What are key features in the pathophysiology of axial spondyloarthrtitis?
- genetic susceptibility (HLA-B27)
- IL-23 binding to T-cells resulting in IL-17 production
- IL-17 can also result from chronic gut or skin inflammation
- IL-17 acts on epithelial, endothelial and fibroblasts resulting in synovitis
- IL-7 can act on osteoclasts resulting in bone erosion
- new bone forms at sties of mechanical stress (SIJ, vertebrae)
What is the most common extra-articular manifestation of axial spondyloarthrtitis?
Anterior uveitis
Does MRI or x-ray findings of sacroiliitis have a greater association with axial spondyloarthrtitis?
X-ray has likelihood ratio of 20 (MRI = 9)
What % of HLA-B27+ individuals develop axial spondyloarthrtitis?
5%
What are MRI features of axial spondyloarthrtitis?
Subchondral bone marrow oedema on STIR = active inflammation
Erosions, sclerosis, ankolysis, fatty lesions on T1 = post inflammatory
Synovitis, enthesitis
What is the treatment for axial spondyloarthrtitis?
1st line:
- NSAIDs
- PT
- if has primarily peripheral disease can consider DMARDs (sulfasalazine, methotrexate) or local steroids (DMARDs have no effect for axial disease)
2nd line: failed 12/52 of therapy
- TNFa blocker: adalimumab, certolizumab pegol, etanercept, golimumab, infliximab
- IL-17 blocker: secukinumab
- JAK inhibitor: tofacitinib, upadacitinib
What are predictors of response to biologic therapy in axial spondyloarthrtitis?
- shorter disease duration
- younger age
- high baseline inflammatory markers
- worse inflammation on MRI
- less functional impairment at baseline
- HLA-B27+
What biologics for axial spondyloarthrtitis should be avoided in IBD?
- secukinumab
- etanercept
What biologic should be used for axial spondyloarthrtitis if IBD or uveitis present?
TNFa mAb: adalimumab, certolizumab pegol, golimumab, infliximab
NOT etanercept in IBD
What is the diagnostic criteria for psoriatic arthritis?
Peripheral or axial arthritis or anthesitis + 3 points from:
- Current skin psoriasis (2 pts)
- Prior or FHx of skin psoriasis (1 pt)
- dactylitis (1 pt)
- nail changes (1 pt)
- RF negative (1pt)
- juxta-articular new bone on x-ray (1 pt)
What are the five distinct patterns of joint involvement of psoriatic arthritis?
- Asymmetric oligoarthritis (most common)
- Symmetric polyarthritis
- Spondyloarthritis (assymetrical, asymptomatic)
- DIPJ with nail disease (pitting oncholysis)
- Arthritis mutilans (shortening of bone)
In what disease do you see a pencil in cup deformity?
Psoriatic arthritis (arthritis mutilans)
How is psoriatic arthritis treated?
- NSAIDs
- intra-articular steroids (not usually systemic)
- If peripheral: methotrexate, sulfasalazine, leflunomide
- Anti-TNFa: adalimumab, certolizumab pegol, etanercept, golimumab, infliximab
- Anti-IL-17: secukinumab, ixekizumab
- Anti-p40 subunit IL-12/23 = ustekinumab
- Anti-p19 subunit IL-23: guselkumab
- JAKi: tofacitinib, upadacitinib (Axial involvement)
What DMARD has activity for all manifestations of psoriatic arthritis?
TNFi
(not etanercept for IBD or uveitis)
What are the safety considerations for JAKi?
- VTE
- major CV events
- malignancy (haem, lung)
- shingles risk
What are clinical features of reactive arthritis?
Sterile arthritis following a remote infection 1-4/52 prior
Asymmetric, oligoarticular, lower limb
Enthesitis
Dactylitis
Sacro-iliitis
Extra-articular:
- skin: keratoderma blenorrhagica, circinate balanitis, mouth ulcers
- ocular: conjunctivitis, uveitis
- genito-urinary: aseptic urethritis, cervicitis, prostatisit
- constitutional symptoms
Classic triad: arthritis/urethritis/conjunctivitis
What organisms have been associated with reactive arthritis?
Chlamydia trachomatis
Shigella spp
Salmonella spp
Campylobacter
Yersinia
How is reactive arthritis treated?
- treat underlying infection
- NSAIDs
- IA steroids
- systemic steroids if unwell
- Sulfasalazine for chronic symptoms
How should IBD associated apondyloarthritis be treated?
- caution with NSAIDs
- Sulfasalazine, anti-TNF or IL-23 blockade for peripheral joints
- Anti-TNF for axial
(avoid IL-17 blockade and entanercept)
What are the 3 pillars of systemic sclerosis?
- autoimmunity
- vasculopathy
- interstitial fibrosis
What are clinical features of diffuse cutaneous systemic sclerosis?
- Raynauds (short history)
- Rapid onset skin changes leading to contractures
- skin of trunk and proximal limbs
- tendon friction rubs
- constitutional symptoms
- early onset organ involvement (lung, kidney)
- Scl-70 antibodies (ILD)
- anti-RNA polymerase III antibodies (renal crisis)
- ANA with nucleolar pattern
What are clinical features of limited cutaneous systemic sclerosis?
Previously CREST
Calcinosis
Raynauds (years)
Oesophageal dysmotility
Skin changes (upper limb and face)
Telangiectasia
Anticentromere antibodies
What is the most common cause of death in systemic sclerosis?
Pulmonary fibrosis
What therapies are indicated for the treatment of skin thickening in systemic sclerosis?
-Methotrexate (2nd line is mcyophenylate, cyclophosphamide)
- PT
- OT
How should ILD be screened for in systemic sclerosis?
- All patients get PFTs and HRCT at baseline
- diffuse get serial PFTs every 3-4 months for 3-5 years the annually
- limited get annual
How should ILD be treated in systemic sclerosis?
- mycophenylate (2nd line is cyclophosphamide)
- anti fibrotic = nintedanib
- tocilizumab if systemic inflammation
What type of pulmonary hypertension occurs in systemic sclerosis?
Type 1 = due to vascular remodelling
Type 2 = due to left heart dysfunction from myocardial involvement
Type 3 = due to ILD
Type 4 = due to antiphospholipid antibodies
What is the most common cause of pulmonary hypertension on systemic sclerosis?
Pulmonary artery hypertension (type 1)
What indicates a role for right heart catheter study to evaluate for pulmonary hypertension in systemic sclerosis?
DLCO <70% predicted + FVC/DLCO > 1.8
OR
proBNP > 210
What are features of a sclerodermic renal crisis?
- abrupt onset of hypertension
- normal urine sediment/mild proteinuria
- progressive renal failure
- can be triggered by corticosteroids
- onion skin appearance on histology
Severe:
- microangiopathic haemolytic anaemia + thrombocytopenia
- heart failure and flash pulmonary oedema
- blurred vision (retinopathy)
- headache, fever, malaise
- encephalopathy, seizure
- pericardial effusion
How is scleroderma renal crisis treated?
- ACEi (captopril)
- IV nitroprusside if CNS involvement
How is Raynaud’s treated?
- treat underlying cause (cryoglobulinaemia)
- cold avoidance
- smoking cessation
- caffeine cessation
- hand skin cares
- keeping warm during procedures
- nifedipine (2nd line = ARB, sildenafil)
- severe = IV prostacyclin
How should rheumatological digital tip ulcers be treated?
- cold avoidance
- vasodilator therapy (IV iloprost, sildenafil, bosentan)
- analgesia
- wound care
How should rheumatological PIP ulcers be treated?
wound care
How should calcinosis be managed?
wound care/debridement if ulcerate
How should critical digital ischaemia be managed?
- urgent admission
- establish and treat cause
- IV prostaglandin
How is faecal incontinence treated in systemic sclerosis?
- exclude overload
- stool firming + laxatives
What are indciations for HSCT in systemic scleroderma?
No smokers non responsive to standard treatment:
- diffuse in first 5 years with moderate organ involvement
- limited with progressive visceral involvement
What are the 4 types of idiopathic inflammatory myopathies?
- polymyositis
- dermatomyositis
- inclusion body myositis
- immune mediated necrotising myopathy
What are the shared features of idiopathic inflammatory myopathies?
Proximal skeletal muscle weakness
Immune mediated muscle inflammation or necrosis
What is the pattern of muscle weakness in dermatomyositis and polymyositis?
Symmetrical proximal muscles weakness:
- deltoids, hip flexors, neck flexors
- diaphargmatic and intercostals
- striated muscle of upper 1/3 of oesophagus
What rashes can be seen in dermatomyositis?
- gotron’s papules (scaling + erythema over hand joints)
- shawl sign (photodistributed poikiloderma)
- helitrope rash
- v sign
- periungal erythema, ragged cuticles
What is the significance of MDA-5 antibodies in dermatomyositis?
- can be amyopathic
- higher risk for ILD
- increased risk of malignancy
What are clinical features of inclusion body myositis?
- insidious onset of asymmetric muscle weakness
- quads often involved
- distal > proximal
- muscle atrophy
- elevated CK
- less responsive to steroids
What feature differentiates statin myopathy from immune mediated?
Myopathy persisting despite statin withdrawal suggests immune mechanism
Statins are recognised trigger for immune mediated necrotising myopathy (anti-HMGCR antibodies)
What key immune mechanisms contribute to dermatomyositis?
Autoantibodies activate complement, deposits in vasculature and mediate capillary necrosis, perivascular inflammation and perfasicular atrophy
What key immune mechanisms contribute to polymyositis
CD8 T-cell responses against molecules
What immune mechanisms contribute to inclusion body myositis?
Accumulation of antigens due to protein misfolding drives KLRG1+T-cell responses
Plasma cells make anti-cN1A antibodies
What is the key immune cell in immune mediated necrotising myopathy?
Macrophages
What are histopathological features of the following:
- dermatomyositis
- polymyositis
- inclusion body myositis
- immune mediated necrotising myopathy
dermatomyositis:
- perifasicular mononuclear cells
- perifasicular atrophy
polymyositis:
- lymphocytic invasion into myofibre
inclusion body myositis:
- vacuoles rimmed with basophilic granules
immune mediated necrotising myopathy:
- muscle fibre necrosis with sparse inflammatory infiltrate
What are immunhistochemistry features of:
- dermatomyositis
- Anti-synthetase syndrome
- inclusion body myositis
- immune mediated necrotising myopathy
dermatomyositis:
- MxA positive
- MAC deposited in endomysial capillaries
- perifasicular MHC-I
- MHC-II negative
Anti-synthetase syndrome:
- MxA negative
- MHC-II on myofibres
- perfasicular MAC deposition
inclusion body myositis:
- p62 positive
- CD8 infiltrate
- KLRG1 positive
immune mediated necrotising myopathy:
- p62 positive in sarcoplasm
- diffuse MAC deposition
Which anti-synthetase antibody is associated with mechanics hands?
Anti-Jo-1
What malignancies are associated with dermatomyositis and polymyositis?
DM: cervix, lung, ovaries, pancreas, bladder, CRC, stomach, NHL
PM: lung, bladder, NHL
How are dermatomyositis, polymyositis and immune mediated necrotising myositis treated?
- high dose steroids (80 mg/day) tapered over 1 year
- azathioprine
- methotrexate
- rituximab
How is inclusion body myositis treated?
Limited response to steroids
IVIg for dysphagia
What are clinical features of giant cell arteritis?
- systemic vasculitis of medium and large arteries
- affects age > 50
What is the most common cause of vision loss in GCA?
Anterior ischaemic optic neuropathy (due to occlusion of posterior ciliary arteries, is not pathognomic)
What are the 4 clinical patterns of GCA?
- isolated cranial (headache, jaw claudication, scalp tenderness) = most common
- Symptomatic large vessel vasculitis (claudication, pulseless limb) +/- cranial
- isolated fever/inflammation
- Isolated PMR with vasculitis on imaging
What test has the best utility for diagnosing GCA?
CRP > 20 + platelet > 300
What are ultrasound features of giant cell arteritis?
Halo sign
Luminal narrowing
How is GCA treated?
- visual symptoms: 1 g IV methylpred for 3/7, followed by 40-60 mg/day pred and tapered 15-20 mg/day over 2-3 months then tapered over 1 year
- if no visual symptoms 40-60 mg/day pred
- tocilizumab for large vessel only
What are clinical features of PMR?
- aching, stiffness around, neck, shoulder and hips
- prolonged morning stiffness (key)
- normal muscle strength but limited by pain
- over 50 y/o
How is PMR treated?
- prednisolone 15-25 mg/day for 4 weeks then wean by 2.5 mg every 2 weeks, then by 1 mg/month
- expect response in 48 hours
What are radiographical features of atypical femoral fractures?
- fracture line originates at lateral cortex, is transverse in orientation and becomes oblique as it progresses medially
- localised periosteal or endosteal thickening/flat cortex at fracture site
How are atypical femoral fractures managed?
- stop bisphosphonates and other anti-resorptives (can use teriparatide)
- continue calcium/Vit D
- investigate for secondary cause of osteoporosis and underlying metabolic bone disease
- surgical repair
- muscle strenghthening exercises
What is the leading cause of death in myositis?
CV disease
(accelerated atherosclerosis, myocarditis)
What antibodies are associated with myocarditis?
SRP
MDA-5
Jo-1
PL12
Ro
Antimichondrial antibodies
What are single gene defects associated with SLE?
- complement deficiencies: C1q, C4A and B, C2
- TREX1 gene mutations
- TLR7 gene mutation
What drugs can induce lupus?
Hydralazine (high risk)
Procainamide (high risk)
etanercept
infliximab
interferon-alpha
minocycline
isoniazid
rifampin
phenytoin
penicillamine
quinidine
phenytoin
methyldopa
chlorpromazine
carbamazepine
ethosuximide
propylthiouracil
sulfasalazine
Diltiazem
What are the 3 main types of lupus rashes?
Acute (non-scarring):
- malar rash (spares nasolabial folds)
- diffuse erythema of skin
- photosensitivity
Subacute:
- annular, papulosquamous or both
- photosensitivie
Chronic:
- discoid lupus, can scar
How is SLE arthritis different to RA arthritis?
SLE typically non erosive and non deforming, synovial effusions uncommon and smaller
What is Jaccoud’s arthropathy?
Rare part of lupus
Tenosynovitis, RA- like swan-neck deformity and ulnar deviation (no erosion on X-ray) and deformity reducible
What is the most common cardiac presentation of SLE?
Pericarditis
What is the most common valvular lesion associated with SLE?
Mitral regurgitation
What is Libman Sacks endocarditis?
Verrucous sterile valvular lesions typically on edge of aortic, mitral and tricuspid valves
Seen in SLE
How should antiphospholipid syndrome associated with SLE be managed?
- hydroxychloroquine has anti-thrombotic effect
- aspirin as prophylaxis
- lifelong warfarin after first unprovoked venous or any arterial event
(DOACs shown in meta-analysis to be inferior to warfarin)
What SLE antibodies are high risk for neuropsychiatric lupus?
antiphospholipid antibodies
Anti-ribosomal p antibodies
Anti neuronal antibodies
What CSF features support a diagnosis of neuropsychiatric lupus?
- raised WCC, elevated protein, low glucose
- oligoclonal bands
- anti-dsDNA, anti-neuronal and anti-ribosomal p antibodies
What auto-antibodies are associated with neonatal lupus?
anti-Ro
anti-La
(risk of complete heart block 16-26/40)
What SLE autoantibodies are associated with renal involvement?
Anti-Sm
Anti-dsDNA
What lab measures can be used to measure SLE disease activity?
ESR > CRP
Increased anti-dsDNA
Low C3/C4
(not ANA)
What are the benefits of hydroxychloroquine for SLE?
- decrease flares
- decrease organ damage
- improve survival
- improve mycophenylate response in lupus nephritis
- improve cholesterol profile
- anti-thrombotic
Immunomodulatory NOT immunosuppressive
What is the major side effect of hydroxychloroquine?
Retinal toxicity
When is a renal biopsy indicated in SLE?
- increased serum Cr without alternate cause
- confirmed proteinuria > 1.0 g/24h
- At least 2 episodes in short time period of : proteinuria > 0.5g/24h AND haematuria OR cellular casts
How is lupus nephritis treated?
- Immunosuppression for class III, IV and V (not for I, II or VI) = induction with IV pulsed steroids AND mycophenylate OR cyclophosphamide, maintenance = mycophenylate or azathioprine
- ACEi if proteinuria > 0.5g/day
- Aim BP < 130/80
- statin for LDL > 2.6
- Plasma exchange for thrombotic microangiopathy
What are contraindications to pregnancy in SLE?
- severe pulmonary hypertension (>50)
- severe restrictive lung disease (FVC < 1L)
- advanced renal insufficiency
- advanced heart failure
- prior severe pre eclampsia or HELLP
- stroke in last 6/12
- severe disease flare in 6/12
How can lupus nephritis be distinguished from pre-eclampsia in pregnancy?
- haematuria/active urinary sediment = SLE
- low complement = SLE
- Anti-dsDNA level raised in SLE
- raised liver enzymes and uric acid = pre-eclampsia
Is hydroxychloroquine safe in pregnancy? What immunosupresants are safe?
Yes
Azathioprine
What autoantibodies are associated with rheumatoid arthritis?
- RF (anti-IgG Fc) = more severe + extr-articular
- ACPA (anti-citrullinated proteins = post-translational modification) = severe + destructive, associated interstitial and CV
- anti-PAD4
-anti-CarP
What is RS3PE syndrome?
Pattern of RA:
- remitting, seronegative, symmetric synovitis with pitting oedema
- hand or foot oedema
- tenosynovitis
- good response to glucocorticoids
- paraneoplastic
What is the swan neck deformity of rheumatoid arthritis?
Subluxation of lateral bands of extensor tendons resulting in volar herniation of PIP and and flexion of DIP
What is the boutinniere deformity of RA?
Rupture of PIP through extensor tendon due to tenosynovitis resulting in PIP flexion and DIP extension
What sort of pleural effusion is associated with rheumatoid arthritis?
Exudate (very low glucose, raised protein : LDH, low complement and low pH)
What is felty syndrome?
Extra-articular manifestation of seropositive rheumatoid arthritis:
-splenomegaly
- leukopenia
- lower limb ulcers
- hyperpigmentation
- bone marrow hyperplasia
What cancers are associated with RA?
- lung cancer
- lymphoma
What are radiographic features of RA?
- periarticular soft tissue swelling
- juxta-articular osteoporosis
- marginal erosions
- joint space narrowing
- symmetric involvement
- deformities
What is the most effective DMARD for RA?
Methotrexate
What is the mechanism of action of leflunomide?
Inhitis dihydroorate hehydrogenase (enzyme in pyrimidine synthesis, required for T-cell activation)
Can patients on biologic DMARDs have live vaccines?
No
Which patient group with RA should be started on biologics?
- adverse prognostic markers (autoantibodies, high disease activity, radiographic damage)
- failed 2 course with conventional DMARD
(not first line)
What is the mechanism of action of abatacept?
binds to the costimulatory molecules CD80 and CD86 on antigen-presenting cells (APC), thereby blocking interaction with CD28 on T cells
What biologics are used for the treatment of RA?
TNFi:
- infliximab
- adalimumab
- golimumab
- certolizumab (lacks Fc, safe in pregnancy)
- entancercept (soluble TNF receptor)
Abatacept (CD80 CD86)
Rituximab (anti-CD20)
Tocilizumab (anti-IL-6R)
JAKi:
- tofacitinib
- baricitinib
- upadacitinib
When should RA drugs be tapered?
- when in remission for at least 6 months and should maintain therapeutic dose on at least 1 DMARD
- prefer ceasing sulfasalazine over hydroxychloroquine
- prefer ceasing methotrexate over biologic
What is the cause of gout?
Immune response to precipitation of monosodium urate crystals in and around joint space
How is uric acid formed in humans and what level defines hyperuricaemia?
End product of purine catabolism, conversion of xanthine to urate by xanthine oxidase
> 0.4 mmol/L
What are the two x-linked recessive syndromes associated with gout due to impaired purine salvage?
- Lesch-Nyhan: complete HGPRT1 deficiency
- Kelley-Seegmiller: partial HGPRT1 deficiency
What is the most common cause of hyperuricaemia?
Under-excretion of urate (20% GIT, majority renal) due to transporter mutation or CKD or drugs (diuretics, aspirin)
Where in the glomerulus is urate reabsorbed and secreted?
Proximal tubule
How do gout crystals appear under polarised light microscopy?
intracellular needle-shaped negatively birefringent
How is an acute flare of gout managed?
NSAID or Prednisone or colchicine +/- intra-articular steroid
What are the two classes of urate lowering therapy?
- xanthine oxidase inhibitors:
- allopurinol
- febuxostat - uricosuric agents = inhibit URAT1 and GLUT9 in proximal tubule
- probenecid
- benzbromarone
What is the serum urate target in gout?
< 0.36 (< 0.3 if severe recurrent flares)
What are clinical features of allopurinol hypersensitivity syndrome?
- desquamating rash, fever, eosinophilia, end organ damage
- HLAB*5801 (Han Chinese, Thai)
- increased risk with concomitant thiazide use
When should an underlying primary metabolic disorder in CPPD be investigated for?
In. patients presenting < 55 years
What are features of CPPD in synovial fluid analysis?
- raised WCC, 90% neuts
- rhomboid/rod-shaped crystals
- weak positive bifringence with polarised light
How is CPPD managed?
NSAIDs, prednisone, corticosteroid injection
