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MSK > Crystal Arthropathy > Flashcards

Crystal Arthropathy Flashcards

1
Q

What are common crystal deposition diseases characterised by?

A

Deposition of mineralised material within joints and peri-articular tissue

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2
Q

What is the crystal responsible for gout?

A

Monosodium urate

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3
Q

What is the crystal responsible for pseudo gout?

A

Calcium pyrophosphate dihydrate (CPPD)

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4
Q

What is the crystal responsible for calcific periarthritis/tendonitis?

A

Basic calcium phosphate hydroxy-apatite (BCP)

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5
Q

What are the 2 most common crystal arthropathies?

A

Gout and pseudogout

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6
Q

What fractions of uric acid in the body comes from dietary purines?

A
  • 1/3
  • (2/3 - DNA, RNA, HGPRT)
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7
Q

What is the breakdown process for purines?

A

purines -> hypoxanthine -> xanthine -> plasma urate

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8
Q

How is uric acid excreted from the body?

A
  • 70% via kidneys
  • 30% into the biliary tract (subsequently converted by colonic bacterial uricase to allantoin)
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9
Q

How does hyperuricaemia occur in the vast majority of people with gout?

A

Reduced efficiency of renal urate clearance

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10
Q

What are the 2 causes of hyperuricaemia?

A

Overproduction and under-excretion

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11
Q

What are the underlying causes of overproduction?

A
  • Malignancy e.g lymphoproliferative, tumour lysis syndrome
  • Severe exfoliative psoriasis
  • Drugs e.g. ethanol, cytotoxic drugs
  • Inborn errors of metabolism
  • HGPRT deficiency
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12
Q

What are the underlying causes of under-excretion?

A
  • Renal impairment
  • Hypertension
  • Hypothyroidism
  • Drugs e.g. alcohol, low dose aspirin, diuretics, cyclosporin
  • Exercise, starvation, dehydration
  • Lead poisoning
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13
Q

Why is alcohol thought to increase the risk of gout?

A

As the metabolism of ethanol to acetyl CoA leads to adenine nucleotide degradation resulting in increased formation of adenosine monophosphate, a precursor of uric acid

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14
Q

What is Lesch Nyan syndrome?

A

Genetic HGPRT deficiency

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15
Q

What are the features of Lesch Nyan syndrome?

A

•X-linked recessive •Intellectual disability •Aggressive and impulsive behaviour •Self mutilation •Gout •Renal disease

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16
Q

What is the importance of HGPRT deficiency?

A
  • HGPRT - hypoxanthine-guanine phosphoribosyl transferase
  • Plays a key role in the recycling of the purine bases (hypoxanthine and guanine) in the purine nucleotide pools
  • In absence of HGPRT, the purine bases cannot be salvaged and they are degraded and excreted as uric acid
  • There is also an increased synthesis of purines (presumably to compensate for purines lost) which also contributes to the over-production of uric acid
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17
Q

Who gets gout?

A
  • Predominantly older men
  • Men always > women
  • Men have higher rate levels
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18
Q

How does oestrogen affect uric acid?

A

It has a uricosuric effect making gout very rare in younger women

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19
Q

How does ageing affect prevalence of gout?

A
  • There is an increased in sUA levels mainly due to reduced renal function
  • Increased use of diuretic and other drugs that raise sUA
  • Age-related changes in connective tissues which may encourage crystal formation
  • Increased prevalence of OA
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20
Q

How is gout diagnosed?

A

•History •Examination •Differential Diagnosis •Investigations

21
Q

Where do gout episodes classically occur?

A

The 1st metatarsophalangeal joint

22
Q

What is the history of a gout episode?

A

•Classically overnight onset •May have been on holiday - alcohol and dehydration •Erythema •Unbearably painful •Lasts 5-7 days •If severe - inflammation of the overlying skin •Potentially discharges f chalky material

23
Q

What are tophi?

A

A tophus is a massive accumulation of uric acid

24
Q

Where do tophi occur?

A

•Bony prominences •Ear

25
Q

What is the gold standard in gout investigation?

A
  • Aspirate the joint and look for crystals
  • Aspiration is also important for differential diagnosis of sepsis
  • Don’t usually aspirate the 1st MTP for gout as in so common in that location
26
Q

How is an acute flare of gout treated?

A
  • NSAIDs - some patients cannot take this
  • Colchicine - has anti-inflammatory properties, perhaps slower onset, causes diarrhoea SPECIFICALLY FAVOURED IN GOUT
  • Steroids - useful in renal impairments
27
Q

When does a patient receive prophylactic intervention after a 1st attack of gout?

A

•Single attack of polyarticular gout •Tophaceous gout •Urate calculi •Renal insufficiency

28
Q

What are other indications for prophylactic/long-term treatment of gout?

A
  • Treat if 2nd attack within 1 yr
  • Prophylactically prior to treating certain malignancies
29
Q

How is long-term hyperuricaemia treated?

A
  • Do not treat asymptomatic hyperuricaemia
  • Xanthine oxidase inhibitor e.g. Allopurinol MOST COMMON
  • Febuxostat - option for patients who are unable to tolerate allopurinol, can increase risk of cardiovascular death
  • Uricosuric agents e.g. sulphinpyrazone, probenecid, benzbromarone
  • Canakinumab - IL 1 antagonist, extremely expensive
30
Q

How to allopurinol and febuxostat work?

A

They inhibit xanthine oxidase. Hypoxanthine -x> Xanthine -x> plasma urate

31
Q

At what point should you attempt to reduce the urate level?

A
  • Wait until the acute attack has settled
  • Use prophylactic NSAIDs or low dose colchicine/steroids until urate level normal (poss. with allopurinol treatment)
  • HOWEVER, if already on allopurinol during acute attack, continue treatment
32
Q

What factor is important when using allopurinol?

A

•Adjust allopurinol dose according to renal function •Increase monthly until uric acid <300 and begin to wean off NSAIDs/colchicine

33
Q

Where is pseudogout most commonly seen?

A

The knee

34
Q

Who gets pseudogout?

A

Elderly females

35
Q

What are the features of pseudogout?

A
  • Erratic flares
  • Triggers - trauma, intercurrent illness
36
Q

What is the aetiology of pseudogout?

A

•Idiopathic •Familial •Metabolic

37
Q

What is an x-ray feature of pseudogout?

A

Chondrocalcinosis

38
Q

What are the crystals seen under the microscope in pseudogout?

A

Pyrophosphate crystals

39
Q

What is the management of pseudogout?

A
  • NSAIDs
  • I/A steroids
40
Q

What are the prophylactic therapies for pseudogout?

A

THERE ARE NONE

41
Q

What is polymyalgia rheumatica?

A
  • Inflammatory condition of the elderly
  • Close relationship with giant cell arteritis (GCA)
42
Q

What percentage of patients with polymyalgia rheumatic (PMR) have evidence of GCA?

A

20%

43
Q

What percentage of patients with GCA may have PMR?

A

50%

44
Q

How does PMR present?

A
  • Sudden onset of shoulder +/- pelvic girdle stiffness
  • Rare < 50y
  • Usually > 70y
  • F:M 2:1
  • ESR usually > 45 often 100
  • Anaemia
  • Malaise, weight loss, fever, depression
  • Arthralgia/synovitis occasionally
45
Q

How is PMR diagnosed?

A
  • Compatible history
  • Age > 50
  • ESR > 50
  • Dramatic steroid response
  • No specific diagnostic test
46
Q

What are the differential diagnoses for PMR?

A
  • Myalgiconset Inflammatory joint disease - rheumatoid arthritis
  • Underlying malignancy e.g Multiple myeloma, lung cancer
  • Inflammatory muscle disease
  • Hypo/hyperthyroidism
  • Bilateral shoulder capsulitis
  • Fibromyalgia
47
Q
A
48
Q

What is the treatment for PMR?

A
  • Prednisolone 15mg per day initially
  • 18-24mthcourse
  • Bone prophylaxis - >65 bone protection, <65 dexascan needed first

MSK (28 decks)

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