Gout 1 Flashcards

1
Q

what is gout

A

an inflammatory arthritis caused by the precipitation of uric acid crystals in the joint

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2
Q

what are the 2 possible mechanisms of gout

A
  1. under excretion of urate
  2. over production of urate
    - 90% of patients with primary gout are underexretors
    - higher prevelance in men
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3
Q

what are the risk factors associated with gout

A
  1. male/post menopausal women
  2. metabolic syndrome
  3. diet- high purine intake, alcohol, fructose
  4. drugs- diuretics, low dose aspirin, ciclosporin
  5. increased cell turnover- malignant disease
  6. genetic predisposition
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4
Q

outline the drugs which can decrease renal excretion of urate

A

CANT LEAP
1. ciclosporin
2. alcohol
3. nicotinic acid
4. thiazides
5. loop diuretics
6. ethambutol
7. aspirin
8. pyrazinamide

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5
Q

what are the 4 phases of gout

A
  1. asymptomatic hyperuricaemia
  2. acute flares
  3. painless intercritical segments
  4. chronic polyarthropathy with tophus formation
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6
Q

describe the criteria for classifying gout

A

ACR-EULAR gout classification
- characteristics of symptomatic episodes
- time course of episodes
- clinical evidence of tophus
- serum urate
- imaging evidence of gout related joint damage

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7
Q

what is the ideal range of urate concentration

A
  • 180-300 micromol/L
  • 4mg/dl
  • 0.24 mmol/l
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8
Q

what are urate lowering drugs and how do they work

A
  1. xanthine oxidase inhibitors lower the production of urate in the body
  2. uricosuric drugs increase excretion of uric acid in the urine, reducing plasma concentration
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9
Q

give an example of a xanthine oxidase inhibitor

A

allopurinol

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10
Q

give an example of a uricosuric drug

A

probenecid

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11
Q

what are the EULAR treat to target recommendations for the management of gout

A
  1. serum urate must be measured regularly and urate lowering therapy should be adjusted to attain therapeutic target
  2. serum urate level >6mg/dl should be targeted and maintained
  3. in patients with severe gout, target should be <5mg/dl until clinical remission is achieved
  4. acute attacks should be treated promptly with a antiinflammatory medications, taking safety issues into consideration
  5. prophylaxis against attacks should be initiated and continued for at least 6 months after starting urate lowering therapy
  6. renal function should be assessed at time of diagnosis and monitored regularly
  7. comorbidities may influence therapy and outcomes and should be assessed and managed
  8. modifiable risk factors should be addressed through patient education and support
  9. information about gout and its management should be made readily available to patients
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12
Q

what dietary modifications can be made in patients with gout

A
  1. do not eat high purine content
    - oily fish
    - marmite/yeast extraction
  2. eat small amounts of moderate purine content
    - meat/chicken
    - beans/legumes/peas
    - spinach, cauliflower, asparagus
    - mushrooms
    - wholegrain
  3. eat more low purine content
    - bread, pasta
    - milk
    - eggs
    - other fruits and vegetables
    - butter, cheese, ice cream, chocolate
    - cherries and vitamin c
  4. avoid alcohol entirely
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13
Q

describe the diagnosis of acute gout

A
  1. joint fluid examination under polarised microscopy
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14
Q

describe what occurs in an acute gout attack

A
  1. rapid development of warmth, swelling, erythema and pain in the affected joint
  2. pain escalates to most intense level in 8-12 hours
  3. initial attack is usually monoarticular and >50% of cases involve the first MTP joint
  4. other joints involved in early stage are midfoot, ankles, heels and knees
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15
Q

outline the treatment of acute gout

A
  1. treat as early as possible
  2. patient education
  3. NSAID plus PPI or
  4. colchine or
  5. corticosteroid
  6. consider adjunctive non pharmacological treatment
    - topical ice, rest
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16
Q

what is the role of colchine in the treatment of gout

A
  1. blocks microtubule assembly in neutrophils, decreases phagocytosis ad transport of MSU crystals
  2. affects neutrophil migration into joints by decreasing adhesion molecules on endothelial cells and neutrophils in response to IL1 or TNFa
  3. reduces inflammasome driven actuation by microtubule inhibition, which reduces MSU delivery