Arthritis - OA, RA, Gout, Spondyloarthritides Flashcards
Two ways in which OA can arise
Abnormal biomechanical stress on a normal joint
OR
Normal stresses applied to an inherently compromised joint with abnormal physiology
What is a large risk factor for OA
Genetics!!!
How does bone density influence OA x2
High bone density is a RF for development of hand, hip and knee OA
Low bone density is a RF for more rapid progression of hip and knee OA
What is primary OA?
Involves characteristic locations and most likely due to genetic predisposition (abnormal joint physiology)
What is secondary OA?
When OA occurs at atypical joints (eg. ankle) suspect secondary OA - often abnormal joint stressors such as joint trauma, previous fracture, inflammatory arthropathy (gout)
When does joint trauma usually lead to OA and what sort?
15-20- years after the insult - can therefore be a cause of young-onset monoarticular or pauciarticular (less than 4 joints affected) OA
What type of hand OA is an indicator for subsequent knee OA etc
Multiple Heberden’s nodes - sign of primary OA therefore genetic predisposition to OA elsewhere
What can lead to a very severe form of OA?
Abnormal stresses on abnormal joint morphology - eg. meniscus tear in someone with hand OA, more likely to get severe knee OA
Risk factors for OA x8
Genetics, Race (hip OA especially prevalent in Caucasians) Age Sex (women worse everywhere except hip) Obesity (knee++) Bone density Abnormal joint shape and alignment Joint trauma and usage
Common sites for primary OA
Spine, hip, knee, distal and intermediate IP joints
Presenting manifestations of OA x5
Pain, loss of joint motion and function, minimal morning stiffness, short-lived stiffness after resting
AND absence of systemic symptoms or other system involvement
Pathology behind joint stiffness in OA
Accumulation of hyaluronan and hylauronan fragments in deep layers of arthritic synovium during rest - pushes water out
Joint movement then mobilises hyaluronan from the tissue and improves stiffness symptoms
What do the cartilage changes of OA encourage?
Deposition of crystals (calcium and urate) - in the joints, therefore can have superadded acute pseudogout
What can lead to increased risk of secondary gout with OA
If on long-term thiazide diuretics or have chronic renal impairment - in combination with normal increased risk of deposition of crystals
Cause of pain with use in OA
Mechanical joint damage, enthesopathy (pain at tendon attachment to bone) from ligament or ligamentous attachments
Cause of pain at rest in OA
Inflammation with effusion and joint capsule distention
Cause of pain at night in OA
Intra-osseous hypertension
What causes structural changes in OA?
Bony enlargement, crepitus, deformity, instability and restricted movement
What muscle changes are common in OA?
Muscle weakness or wasting
What is seen on X-ray with OA? x4
Joint space narrowing, marginal osteophyte or “spur” formation and subchondral sclerosis of bone - also bone cysts in intra-articular bone
Lifestyle modifications for management of OA x6
Exercise - both quadriceps strengthening exercises and aerobic activity help
Pool exercise can help reduce joint loading in overweight people
Pacing out physically hard jobs throughout the day
Weight loss
Appropriate footwear
Walking aids
Medication to help OA x5
Analgesics - paracetamol followed by topic NSAIDs or capsaicin
Oral NSAIDs (highly selective COX inhibitors)
Weak opioids
Problems with NSAIDs for OA
GI ulceration risk with typical NSAIDs
Highly selective COX inhibitors - increase risk of MI and stroke you
Problems with weak opioids for OA
Good pain relief BUT CNS side effects eg. headache, constipation and confusion
What are alternative medications for older high-risk OA patients
Nutraceuticals - no renal or GI side effects
eg. Glucosamine or chondroitin sulphate
Injection treatment options for OA x2
Intra-articular steroid injection, quick pain relief that may last few weeks-months (may help for an important event eg. holiday)
Hylauronan preparations are also available - modest prolonged improvement
Surgical treatment for OA
Prosthetic joint replacements - hip and knee especially but now also shoulder, elbow and thumb base
Surgical treatment for mechanical locking in OA
Arthroscopic debridement and lavage - symptomatic improvement from lavage alone can last several months
What does the term “gout” include? x3
An acute attack, the propensity for repeated episodes and also for chronic gouty arthritis
What is the underlying pathology in gout?
Build up of urate which is a breakdown product of purine
What do humans lack which would help with urate?
Uricase - in other mammals it oxidises urate to allantoin - which is readily soluble
What can increase urate levels?
Increased dietary purine intake and increased breakdown of endogenous proteins (cancer treatment or haematological malignancy)
How is urate excreted and how can this affect levels?
Urate is mainly excreted renally - therefore renal problems or drugs affecting renal function can slow down renal urate excretion
Urinary urate in causes of gout
If primarily an increased purine turnover cause then will be high urinary urate - if it is primarily a renal problem then will have low urinary urate
What is the serum concentration of urate needed for urine acid crystals to form?
> 0.42mmol/l (>7.0g/dl)
Upper limit of normal range of serum urate in a) men and post-menopausal women b) pre-menopausal women
a) 0.42mmol/l (>7.0g/dl)
b) 0.36mmol/l (>6.0g/dl)
Epidemiology of gout
Probably about 1% in caucasians
Rare in pre-menopausal women
Higher in pacific islands and new zealanders
Also Malaysia
May be higher in black afro-caribbean ethnic groups
More common in high social classes
Risk factors for gout x7
Age (older) Sex (male, rare in premenopausal women) Obesity Diet (meat and fish increase risk, dairy products reduce risk) Dietary fructose (sweeteners in US) Drugs (thiazide diuretics) Alcohol (beer>>spirits>>wine) Environmental lead exposure
Why is gout rare in pre-menopausal women?
Possibly due to the uricosuric effects of oestrogens
Relationship of alcohol and gout
Strong relationship between beer intake and gout (purines in yeast)
Weak relationship between spirit intake and gout
No relationship between wine intake and gout
What is the relationship between gout and hyperuricaemaia
Hyperuricaemia is needed for gout (crystals cannot form if serum not >0.42mmol) BUT not everyone with hyperuricaemia develops gout
Which joint is most commonly affected in gout?
First metatarsophalangeal joint (base of big toe)
Clinical features of acute gout
Rapid onset of monoarthritis - severe pain and inflammation in joint with overlying skin erythema
Also may have low-grade fever, general malaise and anorexia
What can onset of acute gout follow?
Drinking bout or local trauma
Infection, starvation, introduction or withdrawal of hypouricaemic agents
Progression of acute episode of gout?
Symptoms peak at 24hours
Can resolve sponteanously in 7-10 days if untreated but can also last for several weeks
What are the other most commonly affected joints in gout?
Foot, ankle, knee, wrist, finger and elbow - more commonly peripheral joints because crystals more likely to form in cooler joints
When in the day do gout attacks typically occur?
At night
Gold standard for diagnosing gout and the problem?
Urate crystals in synovial fluid BUT not many people with acute gout are going to want their joint aspirated
Appearance of urate and pyrophosphate crystals on polarising microscopy?
Urate crystals are strongly negatively birefringent on polarising microscopy
- Pyrophosphate are weakly positively birefringent
What DDX needs to excluded with gout?
Septic arthritis
What can chronic gout cause in older people?
Inflammatory arthritis - especially those on diuretics
What deposits can occur in chronic gout?
Crystal deposits (tophi) can develop around the joints or in the skin or cartilage - Chronic tophi gout can also have persistent low-grade fever
Common sites for tophi? x4
Develop around hands, feet, elbows and ears
In who are tophi particularly common?
Older women with secondary, diuretic-induced gout
They may develop without a history of acute gout
What is the composition of tophi?
Chalky deposits of urate embedded in matrix of lipid, protein and calcific debris
What renal complication can arise in gout? Incidence?
1 in 5 with gout over-excrete urate and may develop urate stones
What % of renal stones are pure urate?
5%
What can gout in childhood be a manifestation of?
Rare inherited disorders of metabolism such as Lesch-Nyhan syndrome, G6PD deficiency
Treatment of acute gout
NSAID’s/COX-2 inhibitor + PPI
Treatment of acute gout in those who can’t tolerate NSAIDs - problem with it
Colchicine - high doses can cause gastrointestinal upset such as diarrhoea
Lower doses are generally better tolerated
Other treatment of severe acute gout
Corticosteroids
Can be taken systemically or injected eg. directly into the joint
Lifestyle management for gout
Lose weight, reduce fish and meat intake, increase low-fat dairy intake, reduce alcohol intake and avoid beer
Main treatment for prevention of gout attack
Urate-lowering medication - Xanthine oxidase inhibitors eg. Allopurinol or Febuxostat
What can starting xanthine oxidase inhibitor cause
Can cause an acute attack of gout
Will also prolong an existing attack and therefore shouldn’t be given during one
Two other less common drugs used for preventing gout attacks
Benzbromarone, probenecid and sulfinpyrazone - are uricosuric drugs which work by inhibiting tubular reabsorption - only really used if people can’t take xanthine oxidase inhibitors
How do xanthine oxidase inhibitors work?
Prevent purine breakdown products xanthine and hypoxanthine being converted into urate
Which 4 drugs have been found to lower urate levels - but are not licensed for treatment of gout?
Losartan
Fenofibrate
Atorvastatin
Amlodipine
What happens in pseudogout?
Deposition of calcium pyrophosphate dihydrate (CPPD) crystals in cartilage
Which joints are most commonly affected in pseudogout?
Knees, ankles, shoulders, elbows, wrists or hands
Treatment of acute pseudogout episodes?
NSAIDs or intraarticular steroids
Lifestyle modifications similar to those for osteoarthritis
Prevention of pseudogout
Long-term NSAIDs or colchicine (oral daily for patients with >3 attacks annually)
What is the hypothesised pathology of rheumatoid arthritis?
An antigen in genetically predisposed individual initiates self-perpetuating immune response which cross-reacts with host tissue causing autoimmune synovitis and subsequent hypertrophy - this hypertrophy is the key factor that leads to cartilage and bone destruction - leading to progressive joint damage and disability
What is key effector cell in RA and how?
T-cell it mediates an immune response through a host of cytokines
What are the two key cytokines involved in pathogenesis of RA
TNF-alpha and Interleukin 1
Which genetic component has been found to be significant in RA
HLA-DR4 - established as a marker of prevalence as well as severity
When does RA commonly occur in men?
Rare before age of 30, increasing incidence with age
When does RA commonly occur in women
Steadily increases in incidence from mid-20s to peak incidence between 45 and 75 years
How are joints affected in common presentation of RA
Small joints of the hands and feet are affected symmetrically - predominantly the MCP joints, PIP joints and the wrists in the hand
And then MTP and forefoot joints in the feet
What are 3 less common forms of presentation of RA
Acute monoarticular, palindromic rheumatism and asymmetrical large joint arthritis
What is palindromic rheumatism?
Rare episodic form of RA where pain and inflammation occurs in attacks and between attacks the joints are normal
What is the spinal involvement of RA
Spine is rarely affected apart from cervical spine
5 red flags in RA
Atlanto-axial subluxatoin Amyloidosis Pericarditis Monoarticular flare Eye involvement
What are warning signs of atlanto-axial subluxation in RA? x4
Pain around the occiput, radiating arm pain, numbness or weakness of the limbs and vertigo on neck movement
What can happen if atlanto-axial subluxation is not picked up on in RA?
Sudden death - especially if patients undergo neck manipulation for intubation during surgical procedures
What can amyloidosis in RA cause?
Renal deposition of amyloid can be a features of long standing RA
Signs of renal amyloid deposition in RA
Suspect if increasing leg oedema, proteinuria and worsening renal function
What else can cause renal dysfunction in RA
Gold or penicillamine induced proteinuria
What are signs of eye involvement in RA
Sudden onset of eye pain and increased lacrimation - possible scleritis
What can untreated RA scleritis lead to?
Thinning of sclera and risk of perforation = scleromalacia perforans
Indications of RA in the history
Progressive pattern of joint involvement, stiffness and increased pain after period of inactivity
History of joint swellings
FHx of rheumatological disease
What are acute-phase haemotological responses associated with RA? x4
High ESR or CRP
High platelet count
High serum ferritin
Significance of rheumatoid factor in RA
Can be used to support diagnosis but it is not conclusive as RF is present in a number of conditions
What is a more specific marker for RA than RF?
Anti-cyclic citrullinated peptide (anti-CCP) - more specific and sensitive than RF
What do you see radiologically with RA?
Classical periarticular erosions, joint space narrowing, osteopenia - characteristic and may appear within first 3 years of disease
What can MRI pick up in RA?
Early synovitis and bone oedema - to pick up early disease
DDX of RA x3
Psoriatic disease (look for nail pitting or skin lesions) Polyarticular gout (joint aspiration for crystals) Malignant conditions such as leukaemia esp. in young people
New favoured approach for treating RA?
More aggressive combination of drugs in early disease and then “step down” when disease is under control
Use of NSAIDs in RA?
COX-1 inhibitors leads to GI problems
But selective COX-2 inhibitors have potential CV risks
However still used for symptomatic control - but little effect on joint damage or progression of disease
Other symptomatic treatment of RA
Corticosteroids - mainstay for symptom control in RA
Multiple routes of administration are available, including local intra-articular injections and depot
Orally has quicker onset, can be used whilst waiting for DMARDs to have affect
What is one of the oldest disease modifying anti-rheumatic drugs?
Gold - decline in popularity due to weekly injections, poor oral success and toxicity (skin rash or nephrotoxicity) problems
What is the gold standard DMARD?
Methotrexate
All other DMARDs are compared against this
Excellent side effect profile except for post-dose nausea which can be controlled with folic acid
How does methotrexate work in RA?
Believed to be due to induction of adenosine release to the inflammatory environment (different mechanism to its anti-malignancy effects)
What was the first drug (DMARD) developed specifically for treatment of RA?
Sulfasalazine
Side effects of Sulfasalazine x5
Minor GI upset or skin rashes can occur
As can drug induced hepatitis, cytopenias and Steven-Johnson syndrome. oligospermia
What affects the half-life of sulfasalazine?
Acetylation status - therefore slow acetylators are more likely to develop toxicity
What other drug is often used in combination with other DMARDs
Hydroxychloroquine - anti-malarial, effective in early and mild disease but no protection radiologically therefore often used in combination with other drugs
What is the newest DMARD?
Leflunomide - inhibits de novo synthesis of pyrimidines
When is Leflunomide used in RA?
May be useful in patients who have failed to respond to methotrexate - can be used in combination to improve response
Problem with leflunomide in pre-menopausal women
Has recommended washout period of up to 2 years pre-conception therefore careful planning is needed in premenopausal women
Anti-TNF alpha drugs in RA
Etanercept (human TNF receptor 2-immunoglobulin constant region fusion protein)
Then monoclonal Ab’s to human TNF - infliximab and adalimumab
Shown to be effectively clinically and on radiological progression
Drug targeting interleukin 1 for RA
Anakinra - recombinant human IL-1 receptor antagonist
Best benefit with Anakinra in RA
Modest clinical improvement but striking improvement in radiological progression
Idea behind targeting B-cells in RA?
B-cells help T-cell activation and antigen presentation
Drug targeting B cell in RA?
Rituximab - targets B cell surface marker CD20
Effective at suppressing inflammatory parameters and limiting joint damage in RA
How does Abatacept work in RA?
Targets activation of T cells and disrupts T-cell contribution to inflammatory environment
Been proven to slow disease activity and joint damage in RA (not recommended for use in Britain yet)
Coexisting problems in RA
Life expectancy can be reduced up to 7 years in men and 3 years in women but deaths not due to RA - therefore significant co-morbidities with RA - especially CV, therefore careful monitoring is needed
What are the entheses?
Sites where tendons or ligaments insert onto the bone - inflammation = enthesitis and pathology = enthesopathy
What is ankylosis?
Abnormal stiffening and immobility of a joint due to fusion of the bones
What does spondylo- refer to?
The vertebrae of the spine
What HLA are spondyloarthritides associated with?
HLA B27
In what age human do spondyloarthrides occur in?
Occur in children and adults but spinal involvement is rare in children
What is needed for a diagnosis of Spondyloarthritis (SpA)
Either
a) inflammatory spinal pain
or b) asymmetric or predominantly lower limb synovitis
plus c) any of following: psoriasis, IBD, alternating buttock pain, enthesopathy or sacroilitis
Main SpA’s x6
Ankylosing spondylitis Psoriatic arthritis Reactive arthritis (Reiter's syndrome) Enteropathic arthritis Undifferentiated SpA Childhood SpA
Where are SpA more common?
North America and Europe - prevalence of HLA-B27 is higher here
What is ankylosing spondylitis?
Aseptic inflammatory condition of the joints and entheses of the spine (attachment of ligaments to vertebral bodies) - preferentially affecting axial skeleton and large proximal joints
Incidence of AS
0.2% of population
2% of HLA-B27 population
20% of HLA-B27 population with FHx
Male:Female of AS
Male predominate
2.5-5:1
Males present earlier: 6:1 at 16 years and 2:1 at 30 years
When does AS typically begin
Young adulthood
But symptoms can arise in adolescence or earlier
What is the first symptom of AS usually?
Inflammatory back pain - insidious onset of lower back and/or buttock pain, present >3months, awakes from sleep, early morning stiffness and better with exercise
What often accompanies inflammatory back pain with presentation of AS
Fatigue
What does AS lead to?
Uncontrolled inflammation will lead to progressive stiffness and loss of spinal mobility due to reactive new bone formation from inflammation
What clinical criteria are needed for AS
Inflammatory back pain
Limitation of spinal motion in both sagittal and frontal planes
Limitation of chest expansion
What is seen on radiograph of sacroiliac joints in AS? x4
Erosions in the joint line, pseudowidening, subchondral sclerosis and finally ankylosis
What is definite AS diagnosis
Radiological criteria + >1 clinical criteria
Probable AS diagnosis
3 clinical criteria OR
Radiological criteria without any signs or symptoms of clinical criteria
What is seen in radiograph of spine in AS?
Squaring and “shiny corners” of the vertebral bodies
Later - syndesmophytes and facet-joint fusion
Calcification of lateral and anterior spinal ligaments
What is the incidence of peripheral arthritis with AS?
Up to 30% typically develop it
What sort of peripheral arthritis do you get in AS?
Asymmetrical oligoarthritis affecting leg joints, most commonly the knee
Other features of AS which cause heel pain
Enthesitis - at achilles tendon with associated bursitis and at plantar fascia - highly characteristic of AS but also in other SpA’s
What else can occur in feet in SpA’s including AS
Dactylitis (can occur in hands but usually a toe - causing “sausage toe”) strongly suggestive of SpA
What affects 40% AS patients at some time?
Acute anterior uveitis (iritis) - typically unilateral - causing pain, photophobia and if untreated impaired visual acuity
Radiological progression in AS as recorded with Modified Stoke AS Spinal Score
0 = normal 1 = erosion, sclerosis or squaring 2 = syndesmophyte 3 = bridging syndesmophyte
What bone condition can develop in AS?
Osteoporosis - predisposing to spinal fractures
Key features of psoriatic arthritis?
Psoriasis, inflammatory arthritis, enthesitis, dactylitis and in minority sacroiliitis or spondylitis
What differentiates the arthritis psoriatic arthritis from the other SpA’s?
It is the only SpA in which the small joints of the hands are frequently affected
What is arthritis mutilans?
Osteolysis resulting in destruction of the small joints of the digits with shortening
Features of arthritis in psoriatic arthritis x5
Any type can occur - can be asymmetrical oligoarthritis (50%), predominately small joint (5-10%), rheumatoid pattern (25%), arthritis mutilans (1-5%) or spondyloarthritis (20%)
What % of psoriasis sufferers have some form of arthritis?
5-15%
What are psoriatic nail changes
Pitting, onycholysis and hyperkeratosis - seen in 80% of patients
Features of skin lesions in psoriatic arthritis
Can be subtle - look in scalp and natal cleft
What is reactive arthritis (ReA)?
Aseptic arthritis occur subsequent to an extra-articular infection, typically of GI or GU tract
Initial activation of immune system followed by autoimmune reaction
How long after infection does ReA typically occur?
Usually 1-3 weeks
Pattern of arthritis in ReA?
Asymmetrical oligoarthritis especially affecting the leg joints
What else can you get in ReA?
Enthesitis (achilles tendonitis or plantar fasciitis - as with AS)
Dactylitis
Sacroiliitis
What is Reiter’s syndrome?
ReA accompanied by urethritis, conjunctivitis or mucocutaneous lesions — although ReA is commonly being used to describe all of this
- can’t see, can’t pee, can’t climb a tree
What is keratoderma blennorrhagicum?
A painless papulosquamous eruption on palms or soles -which is a mucocutaneous lesion in Reiters
What other mucocutanous lesions can be seen in Reiters
Circinate balanitis, keratoderma blenorrhagicum and painless lingual or oral ulcers
What is enteropathic arthritis?
Inflammatory arthritis + IBD (esp. UC and Crohns)
How do bowel and peripheral joint problems usually occur in enteropathic arthritis?
Usually occur independently and arthritis may wax and wane over years
What is type 1 arthropathy?
Affects 5% of IBD patients
Oligoarticular arthritis typically affecting the knees - self-limiting without joint deformities, may precede onset of IBD symptoms
What can also occur in type 1 arthropathy?
Enthesitis of achilles tendon and plantar fascia and dactylitis
What is type 2 arthropathy?
Affects 3% of IBD patients
Usually polyarticular arthritis affecting MCP joints but also other joints - usually in migratory fashion
What occurs in 20% of IBD patients
Sacroiliitis and spondylitis
What is undifferentiated spondyloarthritis?
Inflammatory back pain or peripheral large joint arthritis in HLA-B27 positive - without fullfilling criteria for a subtype
What is 1st line treatment for sacroiliitis and spondylitis?
Regular physio and exercise
NSAIDs - naproxen or diclofenac
or COX-2 inhibitors - etoricoxib or celecoxib
What is 2nd line treatment for sacroiliitis and spondylitis?
Oral and IM corticosteroids - should be avoided longterm
Or local into sacroiliac joints
What is 3rd line treatment for sacroiliitis and spondylitis?
Anti-TNF alpha agents
Adjunctive treatment for sacroillitis and spondylitis?
Bisphosphonates, calcium and vit D - improve bone density
Low dose amitriptyine at night to improve sleep and reduce pain
What is 1st line treatment for oligoarthritis and/or enthesitis? x4
Analgesics - paracetamol or codeine-based drugs
Intra-articular or intra-lesional corticosteroid (not weight-bearing tendons)
NSAIDs
Orthotics
What is 2nd line treatment for oligoarthritis and/or enthesitis? x3
DMARDs may be effective if aggressive, erosive or polyarticular disease
Methotrexate may be effective for both skin and joint disease
Sulphsalazine - for both joint and bowel disease in IBD
What is 3rd line treatment for oligoarthritis and/or enthesitis?
If inadequate response to conventional DMARDs - Anti-TNF with etanercept, infliximab or adalimumab - can be very effective for skin and joint disease but not been proven as effective for IBD
What is a neuropathic joint?
Due to diabetes, syphilis - charcot joint - rapid degeneration of bones secondary loss to loss of sensory input
What causes neuropathic joint?
Any disease causes reduced sensation in the foot
Main xray signs of neuropathic joint
Multiple losses of joint space
What part of spine is affected first in AS
Lumbar first and then progress to thoracic and cervical regions
When can you get chest pain with AS
Pleuritic chest pain from involvement of costovertebral joints
When do you get posture changes in AS and what sort?
Later in the disease
Thoracic kyphosis and spinal fusion leading to question mark posture
Cardiac consequence of AS
Aortic regurge
Lung complication of AS
Apical fibrosis - would show on CXR
Pneumonic for raised urea levels related to gout
CAN’T LEAP
Cyclophosphamide/ciclosporin
Aspirin (low dose)
Nicotine/nicotinic acid
Thiazides
Loop diuretics
Ethambutol (TB)
Alcohol
Pyrazinamide (TB)
Pathology of psuedogout
Excessive cartilage pyrophosphate production leading to local calcium pyrophosphate supersaturation and CPPD crystal formation/deposition
What causes acute attack of pseudogout arthritis
Shedding of crystals into joint cavity
What predisposes to pseudogout
Most causes of joint damage eg. osteoarthritis trauma
More rarely - haemachromatosis, hyperparathyroidism, hypomagnesiumia, hypophosphatasia
Provoking factors for pseudogout
Intercurrent illness, surgery, local trauma
Who is pseudogout more common in
Women (2:1) and in the elderly > 60
Acute presentation of pseudogout
Painful swollen joint - red hot and tender with restricted ROM and fever
Features of chronic arthropathy
Pain, stiffness and functional impairment similar to osteoarthritis - bony swelling, crepitus, deformity
Investigations in pseudogout
Microscopy - weak positive bifringent crystals
Plain radiograph - chondrocalcinosis or signs of osteoarthritis
What type of nodes do you get in OA?
Heberdens nodes (DIPs) Bouchards nodes (PIPs)
Later hand features of RA x7
Ulnar deviation as a result of subluxation at MCP joints
Swan-neck deformity (hyperextented PIP and flexed DIP)
Radial deviation of wrist
Z deformity of thumb
Boutonniere deformity (flexion of PIP and hyperextension of DIP)
Trigger finger
Wasting of small muscles in hands and palmar erythema
Surgical options in RA x4
Synovectomy, arthrodesis, arthroplasty or tendon repair
HLA associated with reactive arthritis
HLA-B27 identified in 70-80% of patients
Gender ratio for reactive arthritis
20:1 M:F
Management of arthritis of reactive arthritis
Initially rest with NSAIDs - aspirate effusions then when articular infection excluded give intra-articular steroids if NSAIDs haven’t worked
If initial arthritis management doesn’t work?
Can try sulfasalazine or etanercept (if CI or intolerance to sulfasalazine)
Management of circinate balanitis
1% hydrocortisone cream
Prognosis of reactive arthritis
Most remit completely or have little active disease 6 months after presentation
May still get occasional pain in joints, entheses or spine
Some may get chronic arthritis rarely and some develop ank spon
