Crystal Arthropathies Flashcards

1
Q

What is gout?

A

form of inflammatory arthritis.

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

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2
Q

Natural hx of gout?

A

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

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3
Q

Main features gout

A

pain: this is often very significant
swelling
erythema

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4
Q

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

A

1st metatarsophalangeal (MTP) joint

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5
Q

What other joints can gout affect?

A

ankle
wrist
knee

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6
Q

If untreated repeated acute episodes of gout can result in

A

damage the joints resulting in a more chronic joint problem.

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7
Q

Radiological features of gout include:

A

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

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8
Q

joint space is absent in gout

A

false

relative preservation of joint space until late disease

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9
Q

Describe radiological erosions in gout

A

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

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10
Q

WHat causes gout?

A

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

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11
Q

What causes Decreased excretion of uric acid

A

drugs*: diuretics
chronic kidney disease
lead toxicity

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12
Q

What causes Increased production of uric acid

A

myeloproliferative/lymphoproliferative disorder
cytotoxic drugs
severe psoriasis

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13
Q

Aspirin increases plasma urate levels

A

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

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14
Q

What is Lesch-Nyhan syndrome?

A

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

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15
Q

Describe acute management of gout

A

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

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16
Q

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

A

false

if the patient is already taking allopurinol it should be continued

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17
Q

How should NSAIDs be prescribed in acute gout?

A

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

18
Q

WHat is the main side effect of colchicine

A

diarrhoea

19
Q

NSAIDs has a slower onset of action vs colchicine

A

colchicine has a slower onset of action.

20
Q

Indications for urate-lowering therapy (ULT)

A

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
21
Q

Outline urate lowering therapy

A

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

22
Q

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

A

true

23
Q

When should ULT be commenced after an acute attack

A

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

24
Q

How should allopurinol be prescribed?

A

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

25
Q

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

A

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

26
Q

What type of drug is febuxostat

A

xanthine oxidase inhibitor

27
Q

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

A

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

28
Q

Lifestyle modifications for gout

A

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

29
Q

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

A

true

30
Q

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

A

decrease

31
Q

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

A

true

32
Q

Diagnosis of gout?

A

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

33
Q

What is pseudogout?

A

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

34
Q

What should you exclude in monoarthritis

A

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

35
Q

Pseudogout is strongly associated with

A

increasing age

36
Q

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

A

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

37
Q

Pseudogout joint aspiration

A

weakly-positively birefringent rhomboid-shaped crystals

38
Q

Which joints are usually affected in pseudogout?

A

knee, wrist and shoulders most commonly affected

39
Q

X ray in pseudogout

A

chondrocalcinosis

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

40
Q

Management pseudogout

A

aspiration of joint fluid, to exclude septic arthritis

NSAIDs or intra-articular, intra-muscular or oral steroids as for gout