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Core Conditions - Locomotor > Gout > Flashcards

Gout Flashcards

1
Q

What are the 2 main types of crystal arthritis?

How can they be distinguished from each other?

A
  • sodium urate crystals - seen in gout
  • calcium pyrophosphate crystals - seen in pseudogout

they are distinguished by their different shapes and refringence properties under polarised light with a red filter

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2
Q

Why is it not usually useful to check serum urate levels during an acute attack to diagnose gout?

A

gout results from high uric acid concentration

not all patients with a high blood urate level will develop gout, and having a low blood urate level cannot rule out gout

checking serum urate during an acute attack is not usually useful

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3
Q

Which joint is most commonly affected by gout?

A

first metatarsalphalangeal (MTP) joint of the foot

but it can affect any joint, and can affect multiple joints simultaneously

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4
Q

When diagnosing gout, when can it be obvious and when are further tests needed?

What other diagnosis should be considered?

A
  • if it is the 1st MTP that is affected and other risk factors are present, it is likely to be gout
  • it can be more difficult to diagnose if other joints are affected and a joint aspirate may be needed for diagnosis
  • any joint is warm, red and painful should be considered septic arthritis until proven otherwise
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5
Q

How do urate crystals appear when viewed under red polarised light?

A

they are negatively birefringent (appear yellow)

they appear as needle-shaped crystals

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6
Q

What do calcium pyrophosphate crystals look like under red polarised light?

A

they are positively birefringent (appear blue)

they appear as rhomboid shapes

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7
Q

How can a septic joint aspirate be distinguished from gout or pseudogout?

A

if the joint is septic, there are usually no crystals in the aspirate

the aspirate may appear purulent and will contain raised white cells on microscopy

a culture will also be positive

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8
Q

Who is more likely to be affected by gout?

A

it is more common in men with a M : F ratio of 10 : 1

it affects 1.5% of the population but 10% of elderly men

age of onset is usually between 40 and 60

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9
Q

In what groups is gout rarely seen and why?

Why is incidence increasing in women?

A
  • rarely seen before puberty
  • rarely seen in premenopausal women
  • urate levels in the blood rise naturally with age (starts to rise after puberty)
  • uric acid levels are higher in men than in women until the female menopause
  • incidence is increasing in women due to wider use of thiazide diuretics
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10
Q

What are the factors involved in the aetiology of gout?

A

it is multifactorial

in a genetically susceptible individual, certain circumstances can trigger the condition (usually diet related)

also body size, drugs and socio-economic status are involved

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11
Q

What dietary factors are likely to be involved in triggering gout in a genetically susceptible individual?

A
  • high protein diet, including seafood and red meat
  • alcohol (particularly beer)
  • high sugar intake (particularly high intake of sugary drinks)
  • foods that have a high concentration of purine
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12
Q

How can socio-economic status play a role in the aetiology of gout?

A

it tends to be more prevalent in richer populations

it is called a “rich man’s disease” because of its associations with alcohol and an expensive diet

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13
Q

How can body size and drugs influence gout development?

A

there is a greater risk of developing gout in a larger body size

any diuretic increases risk of gout, but particularly thiazide diuretics

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14
Q

What are the four clinical syndromes resulting from hyperuricaemia?

A
  • acute urate synovitis (gout)
  • chronic polyarticular gout
  • chronic tophaceous gout
  • urate renal stone formation
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15
Q

What type of arthritis is gout usually?

Which joints tend to be affected?

A

it is usually a monoarthritis and is only a polyarthritis in 10% cases

the first metatarsalphalangeal (MTP) joint is affected in >65% cases

it also often affects the DIPs and PIPs

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16
Q
A
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17
Q

How does acute urate synovitis (acute gout) tend to present?

A

tends to present in middle-aged men

there is a sudden onset of agonising pain

with swelling and redness of the first MTP joint

the attack occurs at any time but it is often precipitated by too much food or alcohol, dehydration or by starting a diuretic

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18
Q

How long does an untreated acute gout attack last for?

What is recovery associated with?

A

untreated attacks typically last for 7 days

recovery is associated with desquamation of the overlying skin

(peeling skin)

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19
Q

In severe attacks, what can make gout difficult to distinguish from cellulitis?

How can a diagnosis be made?

A

overlying crystal cellulitis makes gout difficult to distinguish from infective cellulitis

a family/personal history of gout and a raised serum urate suggest the diagnosis

if in doubt, blood and other cultures should be taken

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20
Q

In what types of people is chronic polyarticular gout seen in?

A
  • eldery people on long-standing diuretic treatment
  • renal failure
  • men who have been started on treatment with allopurinol too soon after an acute attack
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21
Q

How does chronic tophaceous gout present differently?

A

individuals have very high levels of urate

the sodium urate forms smooth white deposits / crystals (tophi) in the skin and around the joints

they tend to occur on the ear, the fingers or the Achilles tendon

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22
Q

What can happen to tophi is they are not treated?

What are other features of chronic tophaceous gout?

A

large crystal deposits are unsightly and can ulcerate

there is also chronic joint pain and superimposed acute gouty attacks

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23
Q

Are tophi present in all types of gout?

A

NO

deposits of urate crystals in the skin only tend to occur in long-term, poorly controlled gout

(chronic tophaceous gout)

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24
Q

Why can inflammatory arthritis and synovitis occur in acute gout?

A
  • there is urate crystal deposition in the joints
  • the urate crystals are phagocytosed by neutrophils
  • in this process, these cells release inflammatory cytokines, attracting more neutrophils
  • this sets off an inflammatory reaction that leads to inflammatory arthritis
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25
Q

Which joint is most commonly affected by inflammatory arthritis and synovitis in gout?

Why is the inflammation particularly bad when associated with gout?

A

the MTP of the first toe is most commonly affected

the neutrophils quickly die off, so there is rapid turnover of cells

this accelerates the inflammation

this occurs because the crystals are toxic to the cells

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26
Q

What systemic feature often accompanies a presentation of gout?

A

there are warm, painful tender joints

these are accompanied usually by pyrexia

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27
Q

How can chronic tophaceous gout be identified on an X-ray?

A

periarticular deposits (tophi) lead to a halo of radio-opacity on X-ray

and clearly defined (“punched out”) bone cysts

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28
Q

What factors influence the levels of uric acid in the blood?

A

Uric acid levels depend on the balance between purine synthesis and the ingestion of dietary purines

and the elimination of urate by the kidney and intestine

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29
Q

Why does the levels of purine sythesis and ingestion influence uric acid levels?

A

uric acid is the last step in the breakdown pathway of purines

the last two steps in this pathway are:

conversion of hypoxanthine to xanthine

conversion of xanthine to uric acid

they are both catalysed by the enzyme xanthine oxidase

30
Q

In what form does uric acid travel in the blood?

What happens when levels are high in gout?

A

in the blood, uric acid is mostly found as monosodium urate

in gout, there are extremely high levels of monosodium urate

this high concentration allows for monosodium urate crystal formation

31
Q

What is the clinical limit that defines hyperuricaemia?

A

when levels of uric acid in the blood are >2 standard deviations above the mean

this is a uric acid level >0.4 mmol/L

32
Q

How is uric acid excreted normally by the body?

A
  • uric acid is completely filtered by the glomerulus
  • 98-100% is reabsorbed by the proximal tubule
  • 50% is then secreted by the distal tubule
  • some post-secretory reabsorption takes place
  • the result is around 5-10% of the glomerular load being excreted in the urine
  • around 1/3 of uric acid is eliminated in the faeces
33
Q

In >75% of cases of gout, what is the problem causing it?

A

In >75% of cases, the problem is with excretion of uric acid by the kidney

there is not a problem with overproduction of uric acid (which is a result of overproduction of purine)

34
Q

What % of people with a high uric acid level actually have gout?

A

many people have a uric acid level high enough to cause gout, but live happily without symptoms

only 5% of those with a uric acid level >0.5 mmol/L will have symptoms

35
Q

What is the defect associated with inherited gout?

A
  • absence of the enzyme hypoxanthine guanine phosphoribosyl (HGPRT)
  • overproduction of 5-phosphoribosyl-1-pyrophosphate synthase (PRPP)
  • both of these defects lead to increased purine synthesis, and increased production of uric acid
36
Q

What causes primary gout?

A

it results from an inherited (X-linked) gene

this is either due to excess de novo purine synthesis

or reduced renal excretion of uric acid

37
Q

What are enzyme defecrs resulting in excess de novo synthesis of purines in primary gout associated with?

A
  • gout before the age of 20
  • family history of gout that presents at a young age
  • uric acid lithiasis present at presentation, particularly in a young person
38
Q

What does secondary gout result from?

A

any condition in which there is increased lysis of cells

e.g. chemotherapy treatment

cell lysis releases lots of nucleic acids into the bloodstream

these are subsequently broken down into uric acid

39
Q

What prophylactic treatment is given to chemotherapy patients to prevent secondary gout?

A

xanthene oxidase inhibitor

40
Q

What conditions leading to decreased uric acid secretion cause primary and secondary gout?

A

disorders of uric acid excretion that are idiopathic cause primary gout

this accounts for 75% of all cases of gout

decreased uric acid excretion can occur secondary to thiazide diuretics or chronic renal failure (secondary gout)

41
Q

When do patients often have a second gout attack?

What happens if they are left untreated?

A

most patients have a second attack within 18 months

if they are left untreated , they often suffer more regular attacks as time goes on

42
Q

What other conditions are associated with repeat acute attacks?

A
  • arthritis
  • bursitis
  • cellulitis
43
Q

What features may develop after many acute attacks as part of chronic gout?

A

asymmetrical polyarthritis

after many acute gout attacks, there may be:

  • cartilage and bone erosion
  • deposition of urate crystals, resulting in tophi
  • secondary osteoarthritis
  • restriction of joint movements
44
Q

After how many years are tophi typically seen?

How does the severity of them reflect on severity of disease?

A

tophi are usually only seen after 10+ years of untreated / unresponsive gout

the severity of the tophi, and the rate of joint damage, are proportional to the severity of the disease

45
Q

What do tophi look / feel like?

In what type of gout are they more likely to develop quickly?

A
  • they are usually white with a texture like toothpaste
  • if they get caught on something, the discharge is white and chalky
  • they develop more quickly in secondary gout
  • their appearance helps to differentiate them from rheumatoid nodules
46
Q

What 5 investigations are used in gout?

A

Serum urate:

  • NOT useful in acute setting as it is only raised in 60% cases

WCC:

  • often raised

ESR:

  • often raised

Synovial fluid:

  • negatively birefringent
  • high leucocyte count
  • can exclude bacterial infection

X-ray

47
Q

When might an X-ray be used to investigate gout?

What signs are looked for?

A

used to assess joint damage in patients with long-standing disease

  • “punched out” / “rat bite” erosions - looks like a bite has been taken out of the bone
  • flecked calcifications
48
Q

What other blood tests may be taken when investigating gout?

A

serum urea and creatinine to assess for signs of renal impairment

49
Q

What is the first line treatment for acute gout?

A

NSAIDs

high doses rapidly (within hours) reduces pain and swelling

50
Q

What are the initial doses of 3 NSAIDs that are commonly prescribed for acute gout?

A

NAPROXEN:

  • 750mg immediately
  • then 500mg every 8 - 12 hours

DICLOFENAC:

  • 75 - 100mg given immediately
  • then 50mg every 6 - 8 hours

INDOMETACIN:

  • 75mg given immediately
  • then 50mg every 6 - 8 hours

after 24-48 hours, reduced doses are given for a further week

51
Q
A
52
Q

What medication is used in conjunction with NSAIDs or as a replacement in people who cannot tolerate NSAIDs?

Who should not be given NSAIDs?

A

COLCHICINE

typical dose is 1.2g stat, followed by 600mg every 12-24 hours for up to 2-3 days until symptoms resolve

it is given to people with renal impairment or history of peptic ulceration

it can cause GI upset

53
Q

When may steroids be used to treat acute gout?

A

often prednisolone

effective, but more likely to cause side effects than colchicine or NSAIDs

reserved for second line treatment when the others are contra-indicated or have been ineffective

54
Q

Should allopurinol (or other uric acid lowering drugs) be used for an acute attack?

Why?

A

they are traditionally NOT recommended during the acute attack

they have been thought to make symptoms worse during the attack

recent evidence suggests that if they are started with acute treatment for gout, there is no increased risk of worsening the attack

BUT starting this medication OUTSIDE of an acute attack i_ncreases the risk_ of an attack

55
Q

What triggers should be analysed and removed to try and prevent acute gout attacks?

A
  • alcohol
    • particularly beer as it is high in purines
  • dietary excess
    • including too much food that is high in purines
    • lowering cholesterol and calorie intake
  • fasting or severe dieting
  • drugs - diuretics & uric acid lowering drugs
  • physical activity
  • surgery / trauma
56
Q

Under what conditions should allopurinol be used?

A
  • only when attacks are frequent and severe
  • despite dietary changes
  • or when attacks are associated with renal impairment or tophi
  • or when the patient finds NSAIDs or colchicine difficult to tolerate
57
Q

What medication is sometimes recommended to be taken when starting allopurinol?

Why?

A

a prophylactic course of NSAIDs for the first 2-4 weeks before and 4 weeks after starting allopurinol

starting allopurinol can provoke an acute attack of gout

this will reduce the risk of an attack by 2/3rds

58
Q

How does allopurinol work?

A
  • it blocks the enzyme xanthene oxidase
  • xanthene oxidase converts xanthene to urate
  • this rapidly reduces serum urate levels
59
Q

What should be checked before giving allopurinol?

What initial dose should be given?

A

check renal function as lower doses (50 - 100mg) are required in patients with reduced renal function

start at a low dose of 50-100mg daily

this can be titrated up to an effective dose - maximum of 900mg daily

60
Q

What should be monitored to check the effectiveness of allopurinol?

A

serum urate level should be monitored every 3 weeks

the aim is for serum urate to be <0.36 mmol/L

61
Q

What is pseudogout and how does it usually present itself?

A

deposition of calcium pyrophosphate dehydrate (CPPD) crystals

the crystals tend to deposit themselves in articular cartilage

it usually presents as a monoarthritis of the elderly

62
Q
A
63
Q
A
64
Q

Who tends to be affected by pseudogout?

A
  • it is age related - crystal deposition increases with age
  • slightly more common in women
  • often accompanies osteoarthritis
  • can be secondary to phosphate metabolism disorders
65
Q

Which joint is affected most commonly by pseudogout?

A

it presents as a monoarthritis, typically in the elderly

it usually affects the knee

particularly the menisci and the articular cartilages

66
Q

What are the symptoms associated with an acute attack of pseudogout?

How long does an attack usually last for?

A
  • acute onset of severe joint pain
  • joint swelling / effusion
  • tenderness
  • joint feels warm
  • joint may be erythematous

attacks can last from a few days up to 4 weeks

67
Q

What are the differentials for pseudogout?

A
  • gout
  • JOINT SEPSIS

any red, hot swollen joint is treated as sepsis until proven otherwise

68
Q

What radiographic feature is seen in pseudogout?

A

CHONDROCALCINOSIS

seen as horizontal white lines in the cartilage

most commonly seen on X-rays of the knee

69
Q

What are the 2 different types of chronic presentation of pseudogout?

A

Chronic presentation is more common than acute and includes:

  • persistent sub-acute inflammatory arthritis
    • ​this tends to resemble rheumatoid arthritis
  • very long history, similar to OA - often punctuated by acute attacks
70
Q

Which joints can be affected by pseudogout?

A
  • knees
  • wrists
  • shoulders
  • elbows
  • MCPs
  • hips
  • tarsal joints

severe destruction of joints is rare, but can occur and usually presents with subluxation of the affected joints

71
Q

What is the main investigation used to diagnose pseudogout?

A

JOINT ASPIRATION

fluid is examined under polarised red light for CPPD crystals

these are rhomboid shape and postively birefringent (appear blue)

72
Q

What is involved in the treatment of pseudogout?

How is this different from conventional gout?

A
  • the standard NSAID treatment of gout is not as effective
  • for the acute presentation, intra-articular injections of steroids are effective
  • sometimes systemic steroids are used

Core Conditions - Locomotor (5 decks)

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