Gout Flashcards

1
Q

What are the two main types of crystal arthritis?

A
  1. Sodium urate

2. Calcium pyrophosphate

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2
Q

What is gout?

A

Gout is an auto-inflammatory arthritis associated with hyperuricaemia and intra-articular sodium urate crystals

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3
Q

Who does gout affect?

A

Men > women [5:1]

Very rare in pre-menopausal women

Very rare in young people

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4
Q

What are the risk factors for gout?

A

Rich purine foods i.e. red meat, fish

High saturated fat

Fructose containing drinks

Alcohol misuse

Increasing co-morbidity which promote hyperuricaemia

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5
Q

90% of gout is idiopathic.

Causes of gout can be broadly divided into 3 causes:

i. Impaired excretion of uric acid
ii. Increased production of uric acid
iii. Increased turnover of purines

What are the risk factors for impaired excretion of uric acid?

A

Impaired excretion of uric acid:

=> Elderly

=> Men

=> Post-menopausal women

=> Impaired renal function

=> Drugs i.e. thiazide diuretics, low-dose aspirin

=> Hypertension

=> Lead toxicity

=> Increased lactic acid production from alcohol, exercise, starvation

=> Glucose-6-phosphatase deficiency (interferes with renal excretion)

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6
Q

90% of gout is idiopathic.

Causes of gout can be broadly divided into 3 causes:

i. Impaired excretion of uric acid
ii. Increased production of uric acid
iii. Increased turnover of purines

What are the risk factors for production of uric acid?

A

Increased urate production:

=> Dietary (alcohol, sweetners, red meat, seafood)

=> Drugs i.e. warfarin, cytotoxics

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7
Q

90% of gout is idiopathic.

Causes of gout can be broadly divided into 3 causes:

i. Impaired excretion of uric acid
ii. Increased production of uric acid
iii. Increased turnover of purines

What are the risk factors for increased turnover of purines?

A

Increased turnover of purines (thus increased urate):

=> Myeloproliferative disorders i.e. polycythaemia vera

=> Lymphoproliferative disorders i.e. leukaemias

=> Others i.e. carcinoma, severe psoriasis

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8
Q

What are the characteristics of gout?

A

Acute monoarthropathy with severe joint inflammation.

> 50% occur in metatarsophalangeal joint of the big toe (podagra)

Other common joints affects = ankle, foot, small joints of hand, wrist, elbow or knee

Can be polyarticular

Assoc. with raised plasma urate

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9
Q

What may precipitate attacks of gout?

A

Trauma

Surgery

Starvation

Infection

Diuretics

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10
Q

What is the result of long term urate deposits?

A

Long term urate deposit

=> tophi in pinna, tendons and joints

=> renal disease i.e. renal stones and interstitial nephritis

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11
Q

What are the differential diagnosis for gout?

A

Septic arthritis (exclude in any monoarthropathy)

Reactive arthritis

Haemathrosis

Calcium pyrophosphate deposition (CPPD)

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12
Q

What are the 4 clinical stages of hyperuricaemia?

A
  1. Acute gout
    => followed by asymptomatic inter-critical phase ± a second acute attack within 2 years
  2. Chronic interval gout:
    => acute gout attacks superimposed on low-grade inflammation and potential joint damage
  3. Chronic polyarticular tophaceous gout (rare)
    => chronic joint pain, activity limitation, structure joint damage, frequent flares
  4. Urate renal stone
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13
Q

How does acute gout present?

What are the precipitating factors for acute attack?

A

Middle aged man with sudden onset of agonising pain, swelling and redness of the 1st metatarsophalangeal joint (great toe).

Attack precipitated by purine rich food, alcohol excess, dehydration, diuretic therapy

Recovery assoc. with desquamation of overlying skin

25% of attacks have an additional joint affected other than great toe

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14
Q

What are the investigations for gout?

A
  1. Polarised light microscopy of synovial fluid
    => negatively birefringent urate crystals
  2. Serum urate raised
    (but can be normal)
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15
Q

How do you manage gout?

A

High dose NSAID - rapidly reduces pain and swelling e.g.

Naproxen 750mg
Diclofenac 75-100mg

Colchicine - if NSAIDs contraindicated - effective but slower

Corticosteroids - use in renal failure as NSAIDs + colchicine contraindicated

Rest & elevate joint

Ice packs

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16
Q

What prevention / lifestyle advice is given in gout?

A

Lose weight

Avoid prolonged fasts

Stop alcohol

Avoid purine rich food i.e. red meat and fish

Stop low dose aspirin

17
Q

When is prophylaxis treatment indicated?

A

> 1 attack in 12 months, tophi or renal impairment

=> aim is to reduce attacks and prevent damage caused by crystal deposition

18
Q

How do you treat gout to reduce serum uric acid levels (prophylaxis)?

A

Allopurinol - increasing every 4 weeks

=> Allopurinol is a xanthine oxidase inhibitor - reduces serum urate levels

Febuxostat - alternative if allopurinol contraindicated or not tolerated

=> non-purine analogue inhibitor of xanthine oxidase

=> well tolerated + safer in renal impairment

19
Q

How long do untreated acute gout attacks last?

A

~7 days

20
Q

How is the diagnosis of gout confirmed?

A

A family or personal hx of gout and raised serum uric acid levels

If in doubt do blood and joint fluid culture to exclude sepsis / septic arthritis

21
Q

What is chronic tophaceous gout?

What is the clinical presentation?

A

Persistently high levels of uric acid presents with sodium urate forms tophi (smooth white deposits) in skin, around joints, ears and fingers

=> large deposits can ulcerate

=> chronic joint pain

=> superimposed acute gout attack

=> tophaceous gout assoc. with renal impairment ± long term use of diuretics

=> chronic/acute urate nephropathy / renal stones may be present

*Treat with allopurinol

22
Q

What is the classic presentation of chronic tophaceous gout on X-ray?

A

Periarticular deposits => halo of radio-opacity and clearly defined (punched out) bone cysts

23
Q

What is acute calcium pyrophosphate dihydrate deposition (CPPD)?

A

=> Acute monoarthropathy of larger joints in elderly - leads to cartilage calcification

=> usually spontaneous but can be provoked by surgery, illness, trauma

*term psuedogout no longer used

24
Q

What is chronic calcium pyrophosphate dihydrate deposition (CPPD)?

A

=> Inflammatory RA like symmetrical polyarthritis and synovitis

=> CPPD chronic polyarticular osteoarthritis with superimposed acute CCP attacks

25
Q

What investigation is carried out for calcium pyrophosphate dihydrate deposition (CPPD)?

A

Polarised light microscopy of synovial fluid

=> weakly positive birefringent crystals

Assoc. with soft tissue calcium deposits on xray

26
Q

How is calcium pyrophosphate dihydrate deposition (CPPD) managed?

A

Acute attack: ice packs, rest, aspiration and intra-articular steroids

NSAIDs (+PPI) ± colchicine for acute attack

Methotrexate and hydroxychloroquine for chronic CPP inflammatory arthritis