Gout Flashcards
Epidemiology of Gout?
More common in men then women
Less common in women before menopause- oestrogen has protective effect
Aetiology (cause) of Gout?
Caused by hyperuricemia & acid crystal formation.
Hyperuricaemia is due to:
- Renal under excretion- caused by renal disease or polycystic kidney disease.
- Overproduction of urate - caused by e.g. excess dietary purines or alcohol abuse.
Monosodium urate is a metabolite of purines & is ionised form of uric acid in the liver.
Risk factors:
-over consumption of purines (red meat, fish)
- excessive alcohol
- obesity.
- Drugs e.g. Aspirin, Thiazide dieuretics, ACE inhibitors & alcohol can increase uric acid levels in the body by increasing uric acid reabsorption
Prolonged hyperuricemia leads to urate crystal formation in synovium of joint, inflammation then caused due to phagocytosis of crystals by polymorphonuclear leukocytes.
Presentation of Gout
Pain:
- Extremely painful, red, swollen joint.
- Rapid onset -reach max severity 2-6 hrs & often waking patient in the early morning.
- Extreme tenderness – patient can’t wear a sock or let bedding rest on joint.
- Attack is self-limiting (5-14 days)
Joint pattern:
- Most commonly a monoarthropathy.
- May present as oligo or poly arthritis.
- Most commonly affected joints:
1. First metatarsophalangeal (big toe)
2. Tarsometatarsal (mid foot)
3. Ankle
4. Knee
Other:
- warm, shiny skin
- limited range of movement due to pain
- Tophi- yellow, irregular nodules over joint- found on finger, hangs, elbows, Achilles tendon- features of chronic gout
- occurs in acute episodes
Investigations for Gout
Crystal analysis:
- presence of monosodium urate crystals= gout
- strong negative birefringence- yellow & blue under polarised light
- needle shaped
gram stain & culture
- to rule out septic arthritis
Blood tests:
- Serum uric acid level – test becomes more reliable 2 weeks after an acute gout attack so wait to do this!
- White blood cell count - usually exceeds 2.0 x 10⁹/L = neutrophils
Urine dipstine
- Looks for haematuria = can suggest kidney stones
- People w/ gout at higher risk of developing kidney stones.
Radiological findings of Gout
Ultrasound:
- detects erosions & top
- gout-specific double contour sing- where irate is deposited over hyaline cartilage
X-rays:
- Soft tissue swelling- goes opaque
- bone erosions- described as ‘para-articular (away from joint margin)
1. spherical & deep
2. punched out appearance w/ wide base
3. sclerotic margins
4. overhanging edges
- Tophi- calcified deposits
- Joint space preserved unless ever
NOTE- view images on notes
Management for acute Gout? Conservative, pharmacological & surgical?
Conservative:
- Patient education & lifestyle – weight loss, exercise, diet, alcohol consumption
- Rest & elevate limb
- Avoid trauma to affected joint
- Ice packs, hot water bottle & bed cage.
Pharmacological:
1st line
- NSAIDs at max dose & continue treatment 1-2 days after attack
- Co-prescribe w/ PPI for gastric protection e.g. lansoprazole
- Oral colchicine- depends on patient preference-can be used instead of NSAIDs
2nd line:
- Intra-articular corticosteroids e.g. prednisolone.
- Oral or intra-muscular corticosteroids – can be considered in patients who can’t tolerate NSAIDs or Colchicine & if intra-articular injection is not possible.
- Paracetamol – consider as an added pain relief – not generally recommended as a primary treatment.
- DO NOT STOP Allopurinol or Febuxostat during an acute attack if the person is already on these drugs.
Surgery:
- Joint aspiration & debridement (removal of dead/ damaged tissue)
Management for chronic gout (preventing flare ups)?
Start urate lowering drugs once the attack has resolved:
Allopurinol – first line urate lowering agent.
- It’s an Xanthine Oxidase inhibitor!
- Start at low dose & increase every month until the serum acid level is below 300 micromol/L.
- Dose will be different for people w/renal impairment.
Febuxostat – second line.
-Use if Allopurinol isn’t tolerated or contraindicated.
Colchicine – consider prescribing when starting/increasing the dose of a urate lowering drug.
NSAIDs– use if Colchicine can’t be tolerated by the patient.
Prognosis for Gout?
if untreated:
- go on to develop arthritis
- tophi occurs
- risk of recurrence very common
Allopurinol: when should you prescribe, MOA, side effects, contraindications, drug interaction & advice when starting.
Once gout flare has cleared
- only give if patient has 2 or more flares in a year
- don’t prescribe for 1-off flare up
MOA
- Reduces synthesis of uric acid by competitive inhibition of xanthine oxidase
- Xanthine oxidase converts: Hypoxanthine → Xanthine → Uric acid
- Xanthine oxidase converts Allopurinol → Alloxanthine
- Alloxanthine inhibits xanthine oxidase
Side effects:
- GI disturbance- nausea, vomiting
- allergic reaction
- bleeding & bruising
- stevens-Johnson syndrome- flue like symptoms & red/purple rash that peels
Contraindications
- Pregnancy - safe but only use when no other alternative & disease carries a risk for mother & child.
- Liver disease - monitor & reduce dose.
- Renal disease - monitor & reduce dose.
Drug interactions
- Azathioprine - used in psoriatic arthritis & some connective tissue diseases.
- ACE inhibitors or thiazide diuretics - increases risk of hypersensitivity
- Amoxicillin - increases the risk of skin rash.
Advice when starting:
- Allopurinol exacerbates gout when first started.
- Prescribe NSAIDs (or colchicine) for 1-2 days when starting Allopurinol.
- Don’t stop Allopurinol during a flare up.
- taken after meals & patients need to stay hydrated.
Colchicine: when to prescribe, MOA, side effects, drug interactions
Used if NSAIDs are contra-indicated in acute gout:
- gastric ulcers
- previous or active gastric bleed
Used to reduce chances of gout exacerbation or flare when allopurinol or febuxostat are started
MOA:
- colchicine interferes with WBC recruitment
- prevents microtubule assembly
- disrupts- inflammasome activation, cell chemotaxis, cytokines & phagocytosis
side effects:
- GI- abdominal pain, diarrhoea, nausea
- bone marrow disorders
- menstrual cycle irregularities
Drug interactions:
- Colchicine & Ciclosporin - ciclosporin increases how much colchicine the body absorbs & may reduce speed that the kidneys & liver process colchicine.
