Gout Flashcards
What is gout
Persistent raised plasma uric acid (urate) concentrations this leads to uric acid crystal formation - painful inflammation within joints (big toe)
How does gout occur
Monosodium urate crystals (MSU) deposit in cartilage in the joint space resulting from sustained hyperuriaemia (high levels of uric acid) this leads to an inflammatory response
What are the symptoms of gout
Rapid onset (hrs/days)
Severe pain
Swelling
Redness and warmth
Tenderness in joint
Risk factors of gout
Age
Male
Obesity
Purine rich diet (red meat, seafood, alc)
Renal impairment (CKD)
Hypertension
Drugs (beta blockers, diuretics, ACEi)
Family history of gout
Diagnosis of gout
Gold standard
MSU urate crystal detection in fluid from joint
Observation, X-ray, ultrasound
Lab - serum Uric acid (SuA), CPRC and ESR
When to refer someone with gout to secondary care
URGENT ASAP - septic arthritis - generally unwell, painful hot swollen joint
- Unresponsive to uric acid lowering
- Persistent SE despite Max NSAID
- Gout complications e.g neuropathy
- Gout persists despite uric acid levels being lowered
- young onset ( below 30yrs)
- pregnancy
Gout acute management
Start ASAP for 1-2 weeks and R.I.C.E
1st line NSAIDS + PPI
2nd line colchicine
3rd line corticosteroid
If poor response can combine
Gout chronic management
DONT START during an attack (1-2 weeks after) BUT CONTINUE if already on drugs and a attack occurs
1st line allopurinol
2nd line febuxostat
3rd line benzbromarone
When is long term treatment (chronic) needed for gout
2 + attacks in year
Tophi
Young
CKD And gout
Continuing diuretics (HF) and gout
Uric acid renal stones
Allopurinol MOA
Lowers serum uric acid
Inhibits xanthine oxidase
Deposition of urate crystals in tissue (Tophi) is reversed
Uricosuric drugs (benzbromarone) MOA
Inhibits renal tubules from reabsorbing uric acid
Increase renal excretion and decrease urate levels in serum
Metabolism of purines to uric acid
Uric acid is the end product of purine nucleic acid degradation
1. Adenine and guanine are metabolised through the same pathway
2. Deamination occurs of adenine
3. Ribose-5-P removal
4. BOTH are converted to xanthine
5. Converted to uric acid
6. Uric acid is renally excreted
Colchicine SERIOUS SE
STOP severe nausea and vomiting
SAME day assessment If take too much (even if no SE)
Colchicine Ci and cautions
CI HF
Caution/ low dose - fluoxetine, erythromycin
Renal impairment and statin and elderly
Allopurinol SERIOUS SE
STOP if rash but if mild and resolves can continue if rash again DISCONTINUE
Allopurinol CI and cautions
AVOID azathioprine (inhibits metabolism of azathioprine - accumulation of toxic metabolites)
Dose adjustments in renal impairment
Don’t start during an attack (1-2 weeks after) but if already taking continue
Febuxostat SERIOUS SE
STOP if hypersensitivity
DISCONTINUE do not restart
Febuxostat CI and cautions
AVOID azathioprine
CI - liver impairment, HF, thyroid
