Gout Flashcards
What is gout
Persistent raised plasma uric acid (urate) concentration -> leads to uric acid crystal formation -> painful inflammation within joints (mainly big toe)
How does gout occur
Monosodium urate crystals (MSU) deposit in cartridge in the joint space resulting from sustained hyperuricaemia (high levels of uric acid) this leads to an inflammatory response
What is the metabolism of purines to uric acid
Uric acid is the end product of purine nucleic acid degradation
1. adenine and guanine are metabolised though 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 excreted renally
What are the symptoms of gout
Rapid onset (hours/days)
Severe pain
Swelling
Redness and warmth
Tenderness in joint
What are the risk factors of gout
Age
Male
Obesity
Purine rich diet (alcohol, red meat, seafood)
Renal impairment (CKD)
Hypertension
Drugs (diuretics, ACEi, beta blockers)
Family history of gout
What are the foods with decreased risk of gout
Cherries
Vegetable protein
Vitamin C
Coffee
Dairy
What is the diagnosis of gout
Gold standard - MSU monosodium urate crystal detection in synovial fluid from joint
GP observation
X-ray
Ultrasound
CPR C-reactive protein and ESR
When would you refer 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 (neuropathy)
Gout persists despite Uric acid levels lowered
Young onset below 30
Pregnancy
Needing specialist benzbromarone
What is the acute management of gout
Start ASAP for 1-2 weeks and R.I.C.E
1st line NSAIDS max dose (or cox2inhibitor) &PPI
2nd line colchicine
3rd line corticosteroids
Poor response can combine
What is the chronic management of gout
1st line allopurinol
2nd line febuxostat
3rd line benzbromarone (specialist)
When is long term treatment for gout needed
2+ attacks in year
Tophi
Young
CKD and gout
Continuing diuretics (heart failure and gout)
Uric acid renal stones
When would you start chronic management and how long to wait if an attack of gout happens
DONT start chronic during an attack (1-2 weeks after) BUT continue if already on drug and a attack occurs
Allopurinol MOA
Lowers serum uric acid
Inhibits xanthine oxidase
Deposition of urate crystals in tissue (tophi) is reversed
MOA of uricouric drugs (benzbrolarone)
Inhibit Renal tubules from reabsorbing uric acid
Increase renal excretion and decrease urate levels in serum
Is life long therapy needed
Once sUA targets reached
Reduce ULT dose to maintain targets, check annually, continue lifelong unless modifiable risk factor addressed and cure achieved
Colchine serious SE
STOP severe nausea and vomiting
SAME day assessment if take too much of colchine (even if no SE)
Colchine CI and cautions
C/I heart failure
Caution/ lower dose - fluoxetine, erythromycin, clarithromycin
Renal impairment and stain - elderly
Colchine add info
Normally 2-3 days until symptoms are relieved or vomiting & diarrhoea occurs DONT repeat within 3 days
If c/I can take steroids
Allopurinol dose / special
Don’t start during an attack (1-2 weeks after) but continue if already on drugs and a attack occurs
Take after meals to reduce GI SE
Allopurinol monitoring
sUA monthly to achieve serum urate below targets
Allopurinol SE and SERIOUS SE
GI problems - take after meals
STOP if rash occurs but if it’s mild and resolves can continue if rash occurs again DISCONTINUE
Allopurinol C/I and cautions
AVOID azathioprine (inhibits metabolism of azathioprine - accumulation of toxic metabolites)
Increased risk of hypersensitivity in renal impairment - dose adjustment
Febuxostat dose / special
Don’t start during an attack (1-2 weeks after) but continue if already on drugs and a attack occurs
Febuxostat SE and serious SE
GI problems, Odema
STOP if hypersensitivity
steven-Johnston syndrome
Actue anaphylactoid/ shock DISCONTINUE and DO NOT restart
Febuxostat c/I and cautions
AVOID azathioprine (inhibits metabolism of azathioprine - accumulation of toxic metabolites)
C/I liver impairment, thyroid disorders, heart failure
Increased risk in PT. With CV disease