Crystal arthropathies and OA Flashcards
epidemiology of gout?
common > 60 year old (male > 40)
rare in premenopausal female
Cause of gout
primary
- idiopathic (90% - underexcretion of uric acid)
- rare enzyme deficiencies (hypoxanthin-guanine phosphoribosyltransferase)
secondary
- excess uric acid produce/ intake
- dietary excess (shellfish, liver, kidney, anchoves, turkey, sardine, beer)
- myeloproliferative and lymphoproliferative disorders
- cytolyic therapy
- acidosis (ketosis of starvation/ diabetes)
- extreme exercise, status epilepticus
- psoriasis
decrease uric acid excretion
- renal failure, drugs (flurosemide, aspirin/ alcohol, cytotoxic drugs, thaizide diuretics)
- lead intoxication
- Down syndrome
what are some precipitates of acute gout?
change in pH, temp, initiation of antihyperuricemics, alcohol, dietary excess, dehydration, trauma, illness, sx,
clinical features of gout
single/ recurrent episodes of acute inflammatory arthritis
acute crystal arthritis
- affect small joints of the feet (eg. MTP - podagra)
- ankle, knee
gouty nephropathy
- parenchymal crystal deposition -> acute renal failure
- urate stone formation (radiolucent)
chronic tophaceous arthritis
- urate crystals affect articular, periarticular and non-articular cartilage
o/e: stretch over tophi will see white deposit, hard
diagnosis of gout
joint aspiration**
- negative, brirefringent needle shaped crystals
- > 90% crystals of monosodium urate
xray
- tophi (soft tissue swelling, punched out lesions)
what is the pitfall of using uric acid measurement as dx?
uric acid may fall and rise, and may fall > 30% during acute attack and hyperuricaemia is common may not be gout
pharmcotherapy for mx of gout
acute gout:
NSAIDs,
colchicine/ predinisolone (intra-articular/ musular -> if renal/ CVD/ GI disease/ NSAIDs CI)
chronic gout:
- antihyperuricemic drugs (allopurinol, febuxostat): xanthine oxidase inhibitor
- uricosuric durgs (probenecid, sulfinpyrazone): if intolerant/ failure to allopurinol (CI in renal failure)
what conditions are associated with gout?
HTN
glucose intolerance
hyperlipidaemia
obesity
indications for urate lowering therapy
attack recur within 1 year of first attack OR after 1st attack: - visible tophi - renal impairment - uric acid stones - cannot stop diuretics
what is the aim to reduce serum urate to?
how to prevent precipitate of acute attacks after using urate lowering agents
use colchicine during first few months of urate lowering med
non-pharm mx of gout
lose wt (obese) reduce alcohol intake reduce excessive dietary purine intake identify and treat associated factors (hypertension, hyperlipidemia, hyperglycaemia) withdraw drugs that can precipitate gout reduce alcohol intake avoid dehydration
renal disease secondary to hyperuricemia, what is the tx
low dose allopurinol and monitor Cr
is sx recommended for gout?
surgery is not recommended, as crystal impairs healing (need very good clearing), unless pending rupture
drugs:
allopurinol
moa: inhibit xanthine oxidase > reduce uric acid production by inhibiting oxidation of hypoxanthine and xanthine -> uric acid
se: maculopapular rash, abdom pain, heptotoxicity, SJS, TEN,
CI: acute gout (change in conc. of uric aicd -> worsen/ prolong attack)
Treat with colchicines/ low dose NSAIDs
drugs:
colchicine
use: relief pain in acute gout, prevent recurrent attacks, use when starting urate lowering tx to prevent acute attack
moa: inhibit microtuble polymerization and synthesis by binding to tubulin, inhibit mitosis and cell motility, ihnibit neutrophil migration, in inflamed area, reduce inflame reaction to urate crystals but no effect on urice production/ excretion
se: diarrhoea, n and vomit, rash, myopathy, hypersensitiy
renal impairment/ hepatic impairment can increase SE (reduce elimination)
Start asap (within 24 hours of onset of symptoms) in acute setting, consider if NSAIDs/ corticosteroids CI/ not appropraite
probenecid (drugs)
use: LT tx of gout
moa: increase renal excretion of uric acid by block renal tubular reaborption, no analgesic/ anti-inflam effection
se: rash, nause, vomit, alopecia, urinary frequency, uric acid kidney stones (prevent via keep hydrate)
(prohibited in elite sport as it can block use of other banned substance)
regular check of FBC and renal funciton
start once attack settle (not acute as it can precipitate)
what is pseudogout?
acute inflammatory arthritis due to phagocytosis of IgG coated calcium pyrophosphate dihydrate (CPPD) crystals by neutrophils -> inflame mediators within joint space
cause of pseudogout
commonly idiopathic, age related, metabolic disorder (hypercalcaemia, hypomagnesaemia)
hyperparathyroidism, Wilson’s disease, bartter syndrome, haemochromatosis (excess iron), hypophosphatasia (low ALP), ochronosis (accumulation of homogentistic acid in CT -> blueblack)
dx of pseudogout
jt aspiration
- positive birefringent brick shape crystals
- crystals present in 60% of patients
xray:
- chondrocalcinosis in 75% (rediodensities in fibrocartiliaginous structure eg. knee menisci/ linear radiodensities in hyaline artiuclar cartilage
risk factors for pseudogout
advance OA, old age, neuropathic jts
clinical picture of psuedogout
slower onset then gout and last up to 3 weeks, self limited
commonly polyarticular
asymptomatic: radiological chondorcalcinosis (30% in > 80s)
acute monoarthritis: knee/ elbow/ shoulder
inflammatory polyarthritis: mimic RA (10%)
often affect:
knee, polyarticular wrist, hand (MCP), foot (1st MCP), hip
tx of pseudogout
asymptomatic does not need treat underlying metabolic disorders acute: NSADs, colchicine/ corticosteroids prophylaxis: colchicine, NSAIDs chronic: mtx or hydroxychloroquine
what is OA
deterioration of articular cartilage due to local biomechanical factors and release of proteolytic and collagenolytic enzyme with secondary changes
