Gout

Question 1

what is gout?

Answer 1

purine metabolism disorder

crystal arthropathy from excess levels of uric acid leading to precipitation in joints and other tissue

Question 2

epidemiology of gout

Answer 2

most common inflammatory arthritis across the world
prevalence is increasing
more common in elderly
males more at risk

Question 3

what are the risk factors?

Answer 3

high uric acid levels/ hyperuricaemia 
alcohol
obesity
male
age 
renal disease
dyslipidaemia
chemotherapy
diabetes mellitus

Question 4

what is uric acid?

Answer 4

breakdown product of purines

Question 5

excretion of uric acid

Answer 5

predominantly renally excreted and the rest excreted via GI tract
imbalance between production and excretion of uric acid it may crystallise and deposit in soft tissue and joints

Question 6

what are the main mechanisms for gout development

Answer 6

purine overproduction
increased purine intake
decreased uric acid secretion

Question 7

purine overproduction

Answer 7

when there is increased cell turnover or lysis of cells leading to release of purines and breakdown to uric acid. Causes include myelo- or lymphoproliferative disorders, psoriasis and use of chemotherapy agents

Question 8

increase purine intake

Answer 8

several foods and beverages that are rich in purines and increase the risk of developing gout. includes seafood, red meat, alcohol and fructose-rich beverages

Question 9

decreased uric acid secretion

Answer 9

uric acid is predominantly renally excreted so anything that affects the kidneys can increase the risk of developing gout. Causes include diuretics, acute kidney injury, CKD, ACE inhibitors and diabetes mellitus

Question 10

crystal formation

Answer 10

high uric acid levels leads to supersaturation and precipitation of monosodium urate crystals in soft tissue, joints and kidneys. Monosodium urate crystals precipitate in peripheral joints because they are less soluble at low temperatures

Question 11

shape of urate crystals

Answer 11

forms needle-like crystals that can be detected on plane-polarised light. Characteristically monosodium urate crystals are negatively birefringent

Question 12

symptoms caused by crystal formation

Answer 12

deposition of crystals can occur asymptomatically, such as in chronic gout
acute attacks = crystals trigger an acute inflammatory reaction leading to acutely painful swollen joints

Question 13

classical presentation of gout

Answer 13

acutely painful and swollen joint coming on abruptly

intensity reached within 12 hours and lasts less than 2 weeks if untreated

Question 14

joints affected

Answer 14

typically affects first metatarsalphalangeal joint
other common joints:
- knees
- ankles
- wrists
- finger joints
can affect more than 1 joint at a time = polyarticular gout, this is rarer

Question 15

untreated hyperuricaemia

Answer 15

chronic tophaeous gout
development of multiple tophi - collections of urate crystals in soft tissue
classically located on helix of ear, fingers, toes, prepatellar bursa and olecranon

Question 16

recurrent flares of acute gout

Answer 16

can lead to chronic polyarticular arthritis

Question 17

types of gout

Answer 17

acute monoarticular gout
acute polyarticular gout
chronic tophaeous gout

Question 18

presentation of acute monoarticular gout

Answer 18

joint pain
joint swelling
erythema
most commonly 1st metatarsophalangeal joint

Question 19

presentation of acute polyarticular gout

Answer 19

joint pain
joint swelling
erythema
fingers, toes, wrists, ankles and knees

Question 20

presentation of chronic tophaeous gout

Answer 20

tophi

degenerative arthropathy

Question 21

diagnosis

Answer 21

clinical diagnosis
joint aspiration
serum uric acid
plain radiographs 
screening for cardiovascular and renal disease

Question 22

serum uric acid

Answer 22

levels should be taken 4-6 weeks following acute attack
elevated levels are not diagnostic of gout and normal serum uric acid doesn’t exclude gout
during an acute attack, plasma urate levels often fall

Question 23

joint aspiration

Answer 23

gold standard investigation
often not required
should be completed if there is concern about septic arthritis or where diagnosis is in doubt
send joint fluid for crystal microscopy, microscopy, culture and sensitivities

Question 24

how is gout diagnosed from microscopy of joint fluid?

Answer 24

presence of needle-shaped monosodium urate crystals that are negatively birefringent under plane-polarised light

Question 25

plain radiographs

Answer 25

typically normal in acute gout episodes may show subcorticol cysts or bone erosion can be used to exclude differentials

Question 26

management of gout

Answer 26

acute management and long-term prevention

Question 27

acute management of gout

Answer 27

general advice first line therapy second line therapy

Question 28

general advice for gout

Answer 28

advise rest, ice and elevation of joint weight loss diet discussion alcohol consumption discussed

Question 29

first-line therapy

Answer 29

NSAIDs - naproxen or oral colchicine co-prescribe a PPI for gastric protection if giving NSAID no aspirin!

Question 30

second-line therapy

Answer 30

if NSAIDs or colchicine are ineffective or contraindicated then give short course of oral steroids or intra-articular injection of steroids

Question 31

prevention

Answer 31

urate-lowering drugs should be discussed with all patients diagnosed with gout these drugs should be initiated once an acute attack has resolved

Question 32

which patient groups should be advised to commence urate-lowering drugs?

Answer 32

``` 2 or more attacks within 12 months tophi chronic gouty arthritis arthropathy renal impairment renal calculi young age onset diuretic use ```

Question 33

prevention: first-line therapy

Answer 33

allopurinol | monitor uric acid levels every 4 weeks and dose can be uptitrated in relation to levels

Question 34

aim for uric acid levels

Answer 34

under 300 micromol/L

Question 35

cautions for allopurinol

Answer 35

renal impairment | can cause severe, potentially life-threatening hypersensitivity syndrome

Question 36

allopurinol

Answer 36

xanthine-oxidase inhibitor that prevents conversion of hypoxanthine to xanthine and xanthine to uric acid

Question 37

prevention: second-line therapy

Answer 37

febuxostate if allopurinol contraindicated LFTs need to be done prior to and after commencing febuxostat as it can cause acute liver injury uric acid levels should be monitored every 4 weeks and dose uptitrated in relation to these levels

Question 38

cautions in febuxostat

Answer 38

renal impairment | hypersensitivity to allopurinol and renal impairment may indicate hypersensitivity to febuxostat

Question 39

prevention of acute attacks

Answer 39

consider colchicine cover when starting or increasing urate lowering therapies such as allopurinol or febuxostat to prevent acute attacks. This may continue for 6 months don't stop urate lowering therapies during acute attacks