Crystal Arthropathies Flashcards
what are the two main forms of crystal arthropathies
Gout and Pseudogout
what is gout
pathological reaction to the presence of urate crystals in and around synovial joints
what type of crystal causes gout
monosodium urate monohydrase
what joints are more specifically targeted in Gout
1st MCP swelling is almost pathomnemonic for gout
knee is also common, along with small joints of hands/feet
what is the time course for gout
takes months-years for crystals to grow to a detectable amount in the first place
what proportion of hyperuracaemic patients get gout
5%
what is the gender split with gout
10:1
what are risk factors for gout
male increased serum uric acid increased age metabolic syndromes (insulin resistance, dyslipidaemia, HTN) high alcohol intake - predominantly beer
what are features of secondary gout
primary
Chronic hyperuricaemia resulting from drug therapy or renal impairment
Mainly affects >65 and is the form usually seen in women
In diuretic induced gout, secondary OA is particularly an issue – thought to be due to a genetic definiciency in fighting crystal formation
what factors affect serum uric acid level
IN
1/3 is due to diet
2/3 due to endogenous purine metabolism regulated by xanthine oxidase
OUT
2/3 Kidney Elimination
1/3 gut elimination
what are some factors that predispose to chronic hyperuricaemia (not gout risk factors)
Diminished renal excretion
Renal impairment
Long term diuretics
Low dose aspirin
Increased production of uric acid
Uncommon
Increased purine turnover
Chronic myeloproliferative or lymphoproliferative disorders
Increased de novo synthesis
Most commonly an unidentified enzyme defect
what is the most common reason for gout
90% have an isolated inherited defect in the fractional uric acid excretion impairing the ability to excrete more
when should you suspect a rare specific defect of purine synthesis in a patient with gout
<25 years old
uric stones in urinary tract
strong Fhx of early gout
what is the cause of pseudogout
calcium pyrophosphate crystal deposition in hyaline and fibrocartilage of joints causing chondrocalcinosis
what is the incidence stratified by ages above 55 of pseudogout
rare <55
10-15% in 65-75
30-60% >85
what sites are most affected in pseudogout
knee
wrist
symphsis pubis
how does pseudogout present
acute self limiting synovitis or a chronic arthritis
what metabolic diseases predispose to CPP deposition
Haemachromatosis hyperparathyroidism hypophosphatasia hypomagnesaemia Wilson's disease
what is calcific periarthritis
deposition of hydroxyapatite (main constituent of bones/teeth) into soft tissues - usually periarticular tissues
what is the most common site for calcific periarthritis
supraspinatus tendon (rotator cuff)
how does calcific periarthritis present
can be incidental
may cause severe acute inflammation of the subacromial bursa due to crystal shedding into and around the bursa
what are risk factors for calficic periarthritis
renal failure
hyperparathyroidism
hypophosphatasia
what marker is raised in calcific periarthritis
CRP
how does gout present
rapid onset, monoarticular inflammation
10/10 pain
extreme tenderness
marked swelling
how does an acute attack of gout progress
usually self limiting over 5-14 days with no loss in function
what are the important differentials that need to be excluded when investigating a ?gout
septic arthritis
Cellulitis
how does an acute attack of pseudogout progress
self limiting but takes longer than regular gout - 1-3 weeks until recovery
how does calcific periarthritis present
may be related to trauma
shoulder pain/tenderness with associated swelling and redness
systemic upset/fever common
how does calcific periarthritis progress
self resolves in 1-3 weeks
why may hypouricaemic treatment induce an acute crystal associated attack
Crystal formed in deep tissues like cartilage or tendon can lay dormant for years due to the avascular, aimmune nature of the areas they’re embedded in, but when they’re removed from their sites of origin (an action called crystal shedding) inflammation occurs acutely
Shedding may occur due to local trauma, partial dissolution reducing crystal size (such as in hypouricaemic treatment) or occur as part of an acute phase of an unknown illness
what chronic feature of gout are seen on XR
Osteophyte formation Cyst formation Sclerosis Narowing of joint space (all similar to OA)
gouty erosions - well demarcated punched out defects with retained bone density around the joint space
what features of pseudogout are seen on XR
X-rays will show chondrocalcinosis in hyaline or fibrocartilage with or without the associated structural changes seen in OA
However this is not always evident and its absence does not exclude pseudogout
how do you diagnose gout
crystal analysis of synovial fluid showing strongly negatively bifringent needle-shaped crystals
what gout fluid appear to look like
increased turbidity if acute
chronic = white
how should you investigate a ?gout
aspirate the sample for a cell count, crystal examination and gram stain/culture
Bloods(U+E, FBC, lipids, glucose, ESR)
BP
Urine dip
on crystal examination what should pseudogout crystals appear as
positively bifringent rod/rhomboid shaped crystals
what is the management for an acute gout attack
- Fast acting NSAID (diclofenac/naproxen)
- if not improving oral colchicine
- corticosteroids, articular or PO
what are the side effects for colchicine
severe vomiting/diarrhoea
what is the management for an acute pseudogout attack
Aspiration quickly reduces pain and is usually sufficient
Fluid reaccumulation is common however so an additional intraarticular corticosteroid injection is often also required
Oral NSAIDS and colchinine are also useful but should be avoided in older people
In older people early active mobilisation is the most useful
when is hypouricaemic treatment indicated for gout
chronic hyperuricaemic gout Recurrent attacks of acute gout Tophi Evidence of bone or joint damage Renal disease Gout with greatly elevated serum uric acid levels
what is the treatment for chronic hyperuricaemic gout
allopurinol
when starting someone on allopurinol, how often should they be reviewed + what monitoring is done
uric acid levels every 3-4 weeks and the dose of allopurinol should be increased in 100mg increments (starting dose 100-300mg) until the max dose 900mg is achieved or the levels are normal
why do you not give allopurinol in an acute attack of gout
may prolong it as it will promote shedding of alredy embedded crystals
what are the side effects of allopurinol
Acute attacks may be caused by the drug induction as it encourages crystal shedding due to reduction in the crystal size
Patients should be counselled this and told to continue
concurrent NSAID/colchicine in the first few weeks may mitigate this risk
Extremely Small risk of TEN so if there is ANY risk of a rash patients should be counselled to stop the drug
Interacts with azathioprine (causes myelosuppression) and potentiates warfarin
what is a lifethreatening interaction allopurinol has
azathioprine - causes myelosupression
what are second line options if allopurinol is insufficient + why arent they used more
Uricosuric drugs
Probenecid
Sulfinpyrazone
As effective as allopurinol
But they require several doses per day and the maintenance of a high urine flow (to avoid uric acid crystallisation In the renal tubules
what are second line options for chronic hyperuricaemic gout contraindicated in
Over-producers
Renal impairment
Urolithiasis
what is chronic tophaceous gout
deposition of nodular uric crystal masses
where are nodules formed in chronic tophaceous gout
Extensor sites of fingers Hands Forearms Elbows Achilles tendon Helix of ear
