Arthiritis and other stuff like GOUT Flashcards
Signs of Inflammatory arthitis
New onset joint SWELLING:
Synovial (compressible, tender)
Often red
Warm to touch
Worst in morning / inactivity
Stiffness > 30 mins (usually longer)
Constant or intermittent
Patterns of joint +/- spine involvement vary by arthritis type
Causes of joint inflammation
Inflammatory Arthritis:
RA
Seronegative Spondyloarthritis
Crystal arthrits – gout and pseudogout
Septic arthirits
Egs of Seronegative Spondyloarthritis
Psoriatic
Ank Spond
Reactive Arthritis
Enteropathic – Crohns and Ulcerative Colitis related
RA epidemiology
1% population
2-3x more common in females
Main risks – family history and smoking
Middle age (but any age
What is involved in RA
Symmetrical small joints, hands wrists feet
Big joints involved later, bad prognostic sign if involved at presentation
No spinal involvement
Epidemiology of Seronegative arthiritis
Asymmetrical big joints, with spinal involvement
More common in men
Associated symptoms
Inflammatory bowel, or GI infection, eye inflammation and psoriasis
Nail involvement predicts arthritis in patients with psoriasis
Features of psoriatic arthiritis
RA like
Distal interphalangeal involvement (OA more common)
Mutilans - rare
Dactylitis – sausage digit / toe
Asymetrical large joints + spine
CRP may not be significantly raised
Crystal Arthritis (Gout/) features
Typically acute intermittent episodes joint inflammation
Gout (6x more common in men)
feet, ankles, knees, elbows, hands
Hyperuricaemia
Risks – beer, renal impairment, diuretics, aspirin, FH
Crystal Arthritis Pseudogout features
3 x more common in women
wrists, knees, hands
Typically on background of OA
Chondrocalcinosis on xray
Features of osteoarthiritis
Usually slow onset – months to years
Typically weight bearing joints DIPs, PIPs, thumb bases, big toes
Minimal early morning stiffness (gelling)
No variability to joint swelling
Normal CRP
Clear changes on xray
Example degenerative arthiritis
Osteoarthritis
IA/RA features
Age of onset: Any age
Speed of onset: Rapid- weeks to months
Distribution: Symmetrical polyarthiritis
Joints affected: Small joints of hands and feet
Duration of morning stiffness: Worse in morning for 1 hour
Systemic symptoms: fatigue, fever, night sweats, malaise, myalgia
Swan - neck deformity
Ulnar deviation of fingers
Osteoarthirits features
Age of onset: Later in life
Speed of onset: Slow over the years
Distribution: Initially asymmetrical monoarthirits> polyarthiritis
Joints affected: Weight bearing joints- knees, hips , thumb base, big toe
Duration of morning stiffness: <1hour and worse at the end of the day (after activity)
How do we make a diagnosis
Is it inflammatory?
Visible joint swelling
Elevated CRP
Variable symptoms with flares
Which joint pattern?
Associated symptoms / risks
Psoriasis (particularly with nail involvement)
Inflammatory eye / bowel symptoms
Family / Smoking history (RA)
Tests
RF / CCP+ (RA only). Uric acid between attacks if ?gout
Xrays
Case 1
Mrs Green – 58
Pain in hands
Worsening over 12-18 months
Decreased grip strength
Stiff am – 15 mins
Worst end of fingers, thumbs
Paracetamol and occasional brufen helps a bit
CRP 1.3 (normal range 1-5)
RF 24 (normal range 0-20)
Xray – degenerative changes in DIP joints of both hands and first CMC joints. No erosions.
What is the diagnosis?
What next?
Answer
Brian -45
Presents with acute onset swelling of his right 1st MTP
Woke him from sleep
No trauma
No other joints involved
Pain so bad he can’t put his sock on
Background of high blood pressure
Takes aspirin, bendrofluazide and ramipril
Drinks 15 pints of beer each week at weekends
Blood tests – CRP 56, normal renal function, normal uric acid.
What is the diagnosis?
Why is the uric acid normal?
What are you going to do next?
Answer
Features of crystal arthritis
Crystal Arthritis is the commonest cause of acute joint swelling
Gout most common in men
Pseudogout in women
Easy to diagnose and treat
Miserable for patients
Gout features
Caused by the deposition of monosodium urate crystals within joint
The immunological reaction initiated to try and remove them, leads to acute pain and swelling
Only ‘Curable’ form of inflammatory arthritis
Epidemiology of gout
UK General Practice Research Database – prevalence 1.4% (1999)
7.3% of men aged >75yrs
Overall male : female ratio 5:1
Hyperuricaemia much more common – affects 15% population
Gout prevalence increases with age
Pathogenesis of Gout
Under exretion urate + overproduction urate >
Hyperuricaemia >
Crystal formation & shedding >
Synovial cells > Inflammatory response
What causes under excretion urate in gout
Genetics
Drugs
CKD
Diuretics
Lead toxicity
What causes overproduction of urate in gout
Diet
Alcohol
Metabolic proliferation
Obesity
Psoriasis
Purine rich diet
Causes of Gout
Alcohol - mostly beer
Red meat, shellfish, offal
Soft drifts
Psoriasis
Haematological malignancy
What affects renal clearance of uric acid
Renal impairment (any cause)
Drugs
Low dose aspirin reduces renal clearance by 10%
Diuretics – worse with higher dose
Cyclosporin, TB drugs, theophyllines
Genetics – affects renal clearance of uric acid
Fructose – shares renal uric acid transporter
Essential risk factors for Gout
Renal impairment
Beer
Diuretics
Aspirin
Family History
Fructose
Elderly
Men
Impaired renal function
Clinical features of Gout
Acute episodes
Onset often at night
Resolve spontaneously (quicker with treatment)
Usually recur in a predictable pattern of joint involvement
Typical joints that gout affects
1st MTPJ 90%
Midfoot, ankle, knee, wrist, elbow hand
Periarticular involvement
Olecranon bursitis
Systemic features can occur
Differntial diagnosis for Gout
Septic Arthritis
Trauma
Calcium Pyrophosphate Arthritis
Rheumatoid Arthritis
(Osteoarthritis!)
Investigations for Gout
FBC (expect raised WCC)
U+E
LFT if concern re alcohol
Serum Uric Acid (often normal during acute attack)
CRP
Xray if recurrent episodes or concern re sepsis
Joint aspiration
Joint X ray
4 clinical phases of gout
asymptomatic hyperuricemia,
acute/recurrent gout,
intercritical gout,
chronic tophaceous gout
Acute treatment of Gout
Explain the disease
Advice about lifestyle - alcohol diet weight loss fluid intake
NSAID (short course) unless:
Renal failure
Peptic Ulcer Disease
Some pts with asthma
Colchicine
500ug 2-3 times daily
Corticosteroids
Intra-articular
Oral - low dose (5-10mg short course)
Ice packs
Indication of chronic gout
- Recurrent attacks
- Evidence of tophi or chronic gouty arthritis
- Associated renal disease
- Normal serum Uric acid cannot be achieved by life-style
modifications
Medications for chronic gout
- Allopurinol – Xanthine Oxidase Inhibitor
- Febuxostat – more potent Xanthine Oxidase Inhibitor
- Benzbromarone / Probencid – if allergic / intollerant
Complications of Gout
Disability and misery
Tophi
Renal disease:
Calculi 10 -15%
Chronic urate nephropathy
Acute urate nephropathy (cytotoxics
Mrs Jones – 43
4 week history of pain and definite swelling across MCPs and PIPs both hands
Started suddenly, struggling to use hands
Stiff 1-2 hours am
Tingling in hands at night
Started with pain under toes in last week
Swelling MCPs, decreased fist and tender MCP and MTP squeeze
CRP – 12.7
RF – 38 CCP – 150 (normal range 0-10)
ANA – weak pos
Xrays – normal
What is the diagnosis?
What next?
Answer
For RA
Inflammation x time = damage
Inflammation reversible, but damage not
So our job is to identify and treat inflammation as rapidly as possible, in order to prevent damage and reduce (stop) patients symptoms.
RA pathogenesis
Look at Nazias notes
Clinical presentation of RA
Pain and Swelling of joints
Typically small joints hands, wrists, forefeet
Early morning stiffness (often prolonged)
Sudden change in function
Intermittent, Migratory or Additive involvement
Physical examination for RA
Decreased grip strength / fist formation
Often subtle synovitis – MCPs, PIPs, MTPs, ankles
DIPs are spared
Usually symmetrical
Deformity unusual at presentation
Tests for RA
CRP (+/- ESR)
Rheumatoid Factor
Falsely positive in 10-15% population
70% of patients with RA are positive
Anti-CCP (cyclic citrullinated peptide)
Almost never falsely positive
70% of patients with RA are positive
Selects the subset of patients with most aggressive disease
Joint X rays
X rays in RA
Hands and Feet – many joints on a single Xray
Used as diagnostic, and prognostic tools, and to monitor therapy
Xray changes of RA
Soft tissue swelling
Periarticular osteopenia
Joint space narrowing
Bone erosion
Treatment of RA
to suppress inflammation as completely and quickly as possible once diagnosis confirmed without making our patients ill
Improve symptoms, prevent/reduce damage, prevent premature mortality
Primary care: NSAID, physio, specialist care - primary
Introduce DMARD early - secondary care
Refer to physio, OT, podiatry
Drugs to use for RA
Methotrexate 10-25mg per week
Sulphasalazine 2-3g daily
Leflunomide 10-30mg daily
Hydroxychloroquine 200mg od
Cheap
Limited by toxicity
Efficacy (effective control of disease) in 65-75% patients – significantly higher if earlier
Pro inflammatory cytokines
TNF a
IL-1
Anti inflammatory cytokines
IL-1R a
IL-10
sTNFR
Anti TNF medications that can be used
Infliximab
Etanercept
Adalimumab
Certolizumab
Other medications for RA
Rituximab (anti CD20 – anti-B cell)
Abatacept (anti-T cell)
Tocilizumab (anti-IL-6)
Other treatments for RA
NSAIDs – usually helpful for most inflammatory causes of pain
Colchicine – helpful for crystal arthritis
Steroids – as tablets or injected into inflamed joints
Differential diagnosis for RA
- Psoriatic arthritis
- Infectious arthritis
- Gout
- SLE
- Osteoarthritis
How do you manage flareups of RA
NSAIDS
Glucocorticoids
Complications of RA
Rheumatoid nodules
scleritis
Corneal ulceration
Pericarditis
Increased risk of Heart disease
Carpal tunnel
Pulmonary nodules
What is urate?
metabolite of purine synthesis and the incidence of gout increases withhyperuricaemia(uric acid > 0.45 mmol/L). However, the disease can also occur at completely normal urate levels. Untreated gout can lead to chronic joint damage.
Uric acid is formed as a breakdown product of purines.
Gout pathophysiology
Uric acid has limited solubility in the blood.
When there is too much uric acid in the blood, it can become a urate ion and bind sodium, leading to the formation of monosodium urate crystals
which deposit in areas with slow blood flow, including joints and kidney tubules.
Signs of Gout
Joint inflammation
Gouty tophi
Symptoms of Gout
- Red, tender, hot, and swollen joint.
- Joint stiffness
- Rapid onset severe joint pain
Complications of Gout
Urate nephrolithiasis: there is an association between gout and urate renal stones due to hyperuricaemia
What is pseudogout?
Pseudogout is a form of inflammatory arthritis caused by deposition of calcium pyrophosphate crystals in the synovium.
Pseudogout epidemiology
Mostly women
Most patients affected by acute pseudogout are over the age of 65
RF for pseudogout
- Increasing age: the greatest known risk factor for pseudogout
- Previous joint trauma
- Hyperparathyroidism
- Haemochromatosis
- Acromegaly
- Wilson’s disease
- Hypomagnesaemia
- Hypophosphataemia
Pathophysiology of pseudogout
The deposition of calcium pyrophosphate crystals is thought to trigger synovitis, with the knee, shoulder, and wrist being most commonly affected.
Acute pseudogout
Acute - mainly affects larger joints in the elderly and is usually spontaneous but can be provoked by illness, surgery or trauma
Chronic Pseudogout
Chronic - inflammatory RA-like symmetrical polyarthritis and synovitis
Signs of Gout
Very similar to gout and usually indistinguishable until joint aspiration is performed.
- Joint inflammation: pain, erythema and swelling
- Signs can be monoarticular (1 joint) or polyarticular (several joints)
Symptoms of Pseudogout
- Rapid onset severe joint pain: knee, shoulder and wrist are most commonly affected
- Joint stiffness
Primary investigations for pseudogout
- Joint aspiration:weakly-positively birefringent rhomboid-shaped crystals under polarised microscopy confirm the diagnosis. If any bacterial growth, then patient is likely to have septic arthritis
-
Joint X-ray:chondrocalcinosis (calcification of articular cartilage) is seen in 40% of casesand is highly suggestive of pseudogout but is not diagnostic; theabsenceof chondrocalcinosis doesnotexclude pseudogout
In the knee, this is seen as linear calcifications of the articular cartilage and meniscus
Investigating the underlying cause for pseudogout
Usually only done in young patients:
- Serum bone profile and PTH: investigate for hyperparathyroidism and hypophosphataemia
- Iron studies: investigate for haemochromatosis
- Serum magnesium: investigate for hypomagnesaemia
DD for pseudogout
- Gout
- Septic arthritis
- Rheumatoid arthritis
- Osteoarthritis
Acute management for Pseudogout
- Anti-inflammatory:NSAIDs or colchicine, particularly in polyarticular disease
- Corticosteroid:intra-articularsteroids can be used in monoarticular disease orsystemicsteroids in polyarticular disease
- Cool packs and rest
- Aspiration of the joints - relieves pain
Chronic management for Pseudogout
- DMARDs: e.g. methotrexate and hydroxychloroquine may be considered in chronic pseudogout
- Joint replacement: only indicated in chronic, recurrent cases with severe joint degeneration
Prognosis Pseudogout
Resolution usually happens within a few days of treatment but some can become chronic
