Crystal Arthropathies

Question 1

What is gout?

Answer 1

form of inflammatory arthritis.

form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium

Question 2

Natural hx of gout?

Answer 2

Patients typically have episodes lasting several days when their gout flares and are often symptom-free between episodes. The acute episodes typically develop maximal intensity with 12 hours

Question 3

Main features gout

Answer 3

pain: this is often very significant
swelling
erythema

Question 4

in gout Around 70% of first presentations affect which joint?

Answer 4

1st metatarsophalangeal (MTP) joint

Question 5

What other joints can gout affect?

Answer 5

ankle
wrist
knee

Question 6

If untreated repeated acute episodes of gout can result in

Answer 6

damage the joints resulting in a more chronic joint problem.

Question 7

Radiological features of gout include:

Answer 7

joint effusion is an early sign
erosions
relative preservation of joint space until late disease
no periarticular osteopenia (in contrast to rheumatoid arthritis)
soft tissue tophi may be seen

Question 8

joint space is absent in gout

Answer 8

false

relative preservation of joint space until late disease

Question 9

Describe radiological erosions in gout

Answer 9

eccentric erosions
well-defined ‘punched-out’ erosions with sclerotic margins ina juxta-articular distribution, often with overhanging edges

Question 10

WHat causes gout?

Answer 10

It is caused by chronic hyperuricaemia (uric acid > 0.45 mmol/l)

Question 11

What causes Decreased excretion of uric acid

Answer 11

drugs*: diuretics
chronic kidney disease
lead toxicity

Question 12

What causes Increased production of uric acid

Answer 12

myeloproliferative/lymphoproliferative disorder
cytotoxic drugs
severe psoriasis

Question 13

Aspirin increases plasma urate levels

Answer 13

true
aspirin in a dose of 75-150mg is not thought to have a significant effect on plasma urate levels - the British Society for Rheumatology recommend it should be continued if required for cardiovascular prophylaxis

Question 14

What is Lesch-Nyhan syndrome?

Answer 14

hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency
x-linked recessive therefore only seen in boys
features: gout, renal failure, neurological deficits, learning difficulties, self-mutilation

Question 15

Describe acute management of gout

Answer 15

NSAIDs or colchicine are first-line
oral steroids may be considered if NSAIDs and colchicine are contraindicated. A dose of prednisolone 15mg/day is usually used
another option is intra-articular steroid injection

Question 16

Allopurinol should be stopped in acute flare of gout if alr taking it

Answer 16

false

if the patient is already taking allopurinol it should be continued

Question 17

How should NSAIDs be prescribed in acute gout?

Answer 17

the maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled. Gastroprotection (e.g. a proton pump inhibitor) may also be indicated

Question 18

WHat is the main side effect of colchicine

Answer 18

diarrhoea

Question 19

NSAIDs has a slower onset of action vs colchicine

Answer 19

colchicine has a slower onset of action.

Question 20

Indications for urate-lowering therapy (ULT)

Answer 20

the British Society of Rheumatology Guidelines now advocate offering urate-lowering therapy to all patients after their first attack of gout

ULT is particularly recommended if:
>= 2 attacks in 12 months
tophi
renal disease
uric acid renal stones
prophylaxis if on cytotoxics or diuretics

Question 21

Outline urate lowering therapy

Answer 21

allopurinol is first-line

colchicine cover should be considered when starting allopurinol. NSAIDs can be used if colchicine cannot be tolerated.

the second-line agent when allopurinol is not tolerated or ineffective is febuxostat

in refractory cases other agents may be tried

Question 22

In gout; it has traditionally been taught that urate-lowering therapy should not be started until 2 weeks after an acute attack, as starting too early may precipitate a further attack. The evidence base to support this however looks weak

Answer 22

true

Question 23

When should ULT be commenced after an acute attack

Answer 23

Commencement of ULT is best delayed until inflammation has settled as ULT is better discussed when the patient is not in pain

it is better for a patient to make long-term drug decisions whilst not in pain

Question 24

How should allopurinol be prescribed?

Answer 24

initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 300 µmol/l. Lower initial doses should be given if the patient has a reduced eGFR

Question 25

If prescribing colchicine or NSAIDs with allopurinol (in gout) how long should this be continued for?

Answer 25

The BSR guidelines suggest this may need to be continued for 6 months

Question 26

What type of drug is febuxostat

Answer 26

xanthine oxidase inhibitor

Question 27

In gout, what agents could you try in refractory cases?

Answer 27

uricase (urate oxidase) is an enzyme that catalyzes the conversion of urate to the degradation product allantoin. It is present in certain mammals but not humans in patients who have persistent symptomatic and severe gout despite the adequate use of urate-lowering therapy: Pegloticase (polyethylene glycol modified mammalian uricase) can achieve rapid control of hyperuricemia. It is given as an infusion once every two weeks

Question 28

Lifestyle modifications for gout

Answer 28

reduce alcohol intake and avoid during an acute attack lose weight if obese avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products

Question 29

in gout consideration should be given to stopping precipitating drugs (such as thiazides)

Answer 29

true

Question 30

increased vitamin C intake (either supplements or through normal diet) may increase/decrease serum uric acid levels

Answer 30

decrease

Question 31

losartan has a specific uricosuric action and may be particularly suitable for the many patients who have coexistent hypertension

Answer 31

true

Question 32

Diagnosis of gout?

Answer 32

Gout is diagnosed clinically or by aspiration of fluid from the joint. Aspirated fluid will show: No bacterial growth Needle shaped crystals Negatively birefringent of polarised light Monosodium urate crystals

Question 33

What is pseudogout?

Answer 33

Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium.

Question 34

What should you exclude in monoarthritis

Answer 34

Excluding septic arthritis is essential as this is a potential joint and life-threatening diagnosis.

Question 35

Pseudogout is strongly associated with

Answer 35

increasing age

Question 36

Patients who develop pseudogout at a younger age (e.g. < 60 years) usually have some underlying risk factor, such as:

Answer 36

haemochromatosis hyperparathyroidism low magnesium, low phosphate acromegaly, Wilson's disease

Question 37

Pseudogout joint aspiration

Answer 37

weakly-positively birefringent rhomboid-shaped crystals

Question 38

Which joints are usually affected in pseudogout?

Answer 38

knee, wrist and shoulders most commonly affected

Question 39

X ray in pseudogout

Answer 39

chondrocalcinosis | in the knee this can be seen as linear calcifications of the meniscus and articular cartilage

Question 40

Management pseudogout

Answer 40

aspiration of joint fluid, to exclude septic arthritis | NSAIDs or intra-articular, intra-muscular or oral steroids as for gout