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  1. Clinical presentation (men vs women, clinical story and progression)
    • Men: 1st MTP joint involvement
    • Women: knee presentation more common than foot presentation
    • Can affect any joint in the feet, around the tendons, and less commonly in the knee
    • Clinical story: acute onset of excruciating pain and swelling, often assc. with redness, affects a single joint at a time, lasting for a few days to a week before settling
    • Progression: intermittent flares, untreated symptoms occur more frequently and don't get completely symptom free periods, but severity of flares decreases
    • Initially self-limiting resolving problem
    • Usually mon-articular presentation
    • Hospital in-patients (esp those with CRF) may be poly-articular
  2. Prevalence, M:F ratio
    • Prevalence: 1% of population
    • M>F
    • Affects 1st MTP joint first in 50% of cases
  3. Examination findings
    • Neutrophil driven inflammatory process in the joint: 
    • low grade pyrexia
    • tophi (in chronic untreated gout)
    • Erythema
    • swelling
    • tenderness
  4. Differential Diagnosis
    • septic arthritis
    • Gout
    • pseudogout
  5. Purine Metabolism
    • Nucleic acid --> purine nucleotides --> hypoxanthine --> xanthine --> uric acid (excreted by kidney)
    • First 2 conversions catalysed by HGPT

    • HGPT: hypoxanthine-guanine thosphoylbosyltransferase
    • Uricase: an unsyme that makes uric acid more soluble, but does not exist in humans
    • Uric acid: must be excreted through kidneys in DCT
  6. Lesch-Nyham Syndrome
    • Paediatric syndrome caused by mutation in HGPT 
    • Associated with hyperuricaemia
  7. Normal uric acid levels:
    • ~214 µmol/L – 450 µmol/L 
    • already at the supersaturaed levels in the serum
    • thus an increase above normal levels, uric acid will crystalise out, particularly in joints
  8. Risk Factors: Causes of Increased Uric Acid Syntehsis
    • Purine rich foods: alchoholic drinks (esp beer), seafood (anchovies, sardines, herring), offal, legumes (dried beans), meat extracts (gravy), vegetables (mushrooms, spinach, asparagus, cauliflower)
    • Genetic predisposition: Lesch-Nyhan Syndrome
    • Increased cellular production: fructose (induces cellular production of purines), malignancy, psoriasis, lymphoproliferative disorders
  9. Risk Factors: Causes of Decreased Renal Uric Acid Extretion
    • Renal disease
    • Genetic predisposition: URAT1 genetic pleomorphism (in PCT) e.g. Maori population in NZ
    • Insulin resistance/TIIDM - most important factor in current population - high levels of insulin inhibit ability of URAT1 to excrete uric acid (management is very similar, calorie restriction and weight reduction)
    • Drugs: thiazed diueretics (bendrofluemethiazide), loop diuretics (furosemide), ciclosporin, low dose aspirin
    • Lead toxicity
  10. Pathogenesis of acute attack and triggers
    • Disease is asymptomatic until a trigger causes release of uric acid crystals into the synovial fluid. 
    • The innate immune system recognises the crystals and triggers an acute neutrophilic inflammatory response 
    • Leads to an acute attack (redness, swelling, excruciating pain
    • Triggers: intercurrent infection, acute increase in serum uric acid (e.g. binge drinking, dehydration), acute decreased in serum uric acid (e.g. abstinence, treatment), local trauma
  11. Investigations and possible findings
    • FBC: neutrophil leucocytosis (even more elevated if septic)
    • Renal function: high creatinine (RF for developing gout)
    • Uric acid: may be normal - levels can drop during an acute episode i.e. normal doesn't exclude gout
    • CRP/ESR: both will be high
    • Blood cultures: negative (important)
    • Xray: usually
    • Synovial fluid analysis: very important 
    • Polarised light microscopy: very important
  12. Polarised Light Microscopy
    • Do not memorise which colour for which direction etc
    • Remember: needle shaped crystals, blue to yellow discolouration depending on the direction of the filter
  13. Synovial fluid analysis: Normal, crystal synovitis, septic arthritis
    • Normal: viscous, star, clear, o or low WCC
    • Crystal: low viscosity, straw/opalescent, transucent, WCC + or ++
    • Septic: runny, greenish, opaque, WCC +++
  14. Treatment (matchbox analogy)
    • Matchbox analogy: gout is like having a box of matches inside the joint - if one of them goes up, then all of the matches go up. Thus need different strategies to treat it
    • 1. Acute attacks: i.e. a fire extinguisher, NSAIDs, local steroid infections, oral steroids
    • 2. Prophylaxis: i.e. water to make harder to light - Colchicine 2-3x per day - interferes with neutrophil microtubule formation (makes it more difficult to become activated)
    • 3. Uric acid reduction: if you can decrease the levels, the crystals are progressively reaborbed
    • Education: weight loss, lower calorie intake, lower intake of purine rich foods (esp alochol), treatment modifications (e.g. switch from thiazides to ACEi) NB: can risk a flare up by decreasing levels
    • Allopurinol (1st line)/Febuxostat (2nd line): xanthine oxidase inhibitors
Card Set:
2014-02-15 21:24:51
NRO grout crystal arthropoathy
Gout - flashcards from podcast
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