Crystal Arthropathies Flashcards
gout
inflammatory arthritis associated with monosodium urate crystal deposition in a joint
how does gout usually present
acute monoarthropathy with severe joint inflammation
50% cases in big toe
what is gout called when at MTP of big toe
podagra
gout epidemiology
men more common
prevalence increases with age
gout aetiology
high serum uric acid levels
may be due to renal underexcretion or excessive intake of foods high in protein (alcohol, red meat and seafood)
gout is the end product in protein metabolism
what is gout associated with
cardiovascular disease, hypertension, diabetes mellitus and chronic renal failure
what can exacerbate renal under excretion
diuretics or renal failure
what is the diagnosis of gout based on
identification of crystals and radio graphic findings (not hyperuricaemia alone)
how does the level of uric acid affect gout
level doesnt precipitate gout
rather acute changes in the level of uric acid
what can trigger uric acid precipitation in joints
dehydration, trauma or surgery
(uric acid is water soluble)
is there a genetic predisposition for gout
no evidence of
clinical presentation of gout
intensely painful red, hot swollen joint
rapid onset, lasts for up to 2 weeks if untreated
what may gout mimic
septic arthritis
- inflammatory markers
- felt unwell?
what joints are commonly affected in gout
50% podagra
also knee and ankle
DD of gout
exclude septic arthirits in any monoarthropathy
trauma
seronegative arthritis
CPPD
what are gout tophi
painless white accumulations of uric acid which can occur in soft tissues and occasionally erupt through the skin
chronic polyarticular gout
usually occurs after recurrent acute attacks for more than 10 years
diuretic associated often
tophi present
can resemble RA
what can chronic polyarticular gout result in
destructive erosive arthritis
gout - inflammatory markers
raised a lot
WCC may be raised
gout x ray
- normal in acute attack
- chronic/repeated - erosion, overhanging osteophyte, joint destruction
how can a definitive diagnosis of gout be made
analysing a sample of synovial fluid with polarised microscopy
what befringence do uric acid crystals display
negative
- change from yellow to blue when lined across direction of depolarisation)
managment of acute attack of gout
NSAIDs (symptoms subside 3-5 days)
if cant tolerate - colchicine (slower to work)
corticosteroids
in whichb situations would NSAIDs be contraindicated
eg peptic ulcer
what can colchicine cause in excess quantities
diarrhoea
when are urate lowering therapies given
- recurrent acute attacks (<2 in a 12 month period), joint destruction, renal stones or tophi
how should allopurinol etc be used
- after acute attack has settled down (2 weeks) so as not to cause a sudden change in uric acid levels
- start at low dose and titrate up until serum urate level is achieved (<360micromol/L)
what lifestyle modifications should people with gout do
restrict red meat shell fish and alcohol
weight control
drink lots of fluid
calcium pyrophosphate deposition (CPPD)
an umbrella term use to describe different patterns of disease including pseudogout and chondrocalcinosis
pseudogout
(acute CPP crystal arthritis)
crystal arthropathy causing an acute atthritis by deposition of CPP crystals
where does pseudogout tend to occur
in the large joints of elderly people
course and aetiology of pseudogout
usually spontaenous and self limiting, but can be triggered by illness, trauma or sepsis
chondrocalcinosis
CPP depostion in cartilage in the absence of acute inflammation
where are CPPDs often found
knee wrist and ankle
what can chronic CPPD result in
osteoarthritic changes
what is the cause of CPPD
exact cause unknown
can coexist with hyperPTH, hypothyroidism, renal osteodystrophy, haemachromatosis and wilsons disease
who is CPPD most common in
elderly
what shape are CPP crystals
rhomboid
what befringence do CPP crystals show
postitive - blue to yellow when aligned across direction of polarisation
treatment of CPPD
NSAIDs
colchicine
steroids
rehydration
hydroxyapatite crystal deposition
is a calcium phospahte
causes acute and rapid deterioration
hydroxyapatite deposition in the shoulder
milwaukee shoulder - destructive shoulder arthropathy
hydroxyapatite deposition epidemiology
females
around 50/60
diagnosis of hydroxyapatite deposition
alizarin stain shows red clumps
side effects of allupurinol
rash - must discontinue drug
allopurinol mechanism
xanthine oxidase inhibitor
whaat is another xanthine oxidase inhibitor
Febuxostat
mechanism of uricosuric agents
- block active transport of organic acids leading to reduced reabsorption and secretion of urate - overall reduced net reabsorption
- not suitable in renal impairment of history of renal stones
uricosuric agents
Probenecid, Sulfinpyrazone, Benzbromarone
which uricosuric agent can be used in mild renal impairement
Benzbromarone
what serious drug reaction can allopurinol cause
SJS
what must one ensure whilst taking allopurinol
adequate urine output
what may be a problem with uricosuric agents
- As crystallization of urate in the urine can occur with the uricosuric drugs, it is important to ensure an adequate urine output especially in the first few weeks of treatment
- Patients must increase fluid intake to 2-3 litres daily
what is an additional precuation that may be advised in the first few weeks of uricosuric treatment
render urine alkaline
which drugs antagonise uricosuric drugs in the PT
aspirin and other salicylates
management of patient on allopurinol who develops an acute attack
treat acute attack separately
what ocular manifestation is gout associated with
scleritis
management of scleritis
oral NSAIDs, steroids and steroid sparing agents
