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LOCO 2 > Crystal arthropathies > Flashcards

Crystal arthropathies Flashcards

1
Q

What molecule is innvolved in gout

A

Uric acid

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2
Q

What % of the population have gout

A

1

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3
Q

In which sex is gout more common

A

Men

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4
Q

What crystals are deposited in gout, and where

A

Monosodium urate crystals

Soft tissues

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5
Q

What happens if gout is left untreated

A

Joint destruction

Renal damage

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6
Q

At what age does uric acid rise peak in men and women

A

men– puberty

women– menopause

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7
Q

What is the peak age of onset of gout in men and women

A

men– 4th to 6th decade

women– 6th to 8th decade

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8
Q

How many years are uric acid levels higher before gout onset

A

20

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9
Q

What triggers a gout attack

A

Uncoated crystals or a sudden change in concentration

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10
Q

What are uric acid crystals usually coated in

A

Serum proteins

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11
Q

Can urate crystals cause gout attack if they are found in the synovial membrane

A

No

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12
Q

Which joints does gout usually affect

A

Small, lower extremity joints

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13
Q

What is podagra

A

Inflammation of first MTP joint

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14
Q

Describe the onset of a gout attack

A

begins suddenly

maximum intensity within 8-12 hours

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15
Q

Name some joints commonly affected by gout

A

Knee, ankle, toes, elbow, sometimes shoulder

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16
Q

How does the joint appear/ feel in gout

A

Red, hot, tender, pain starts acuteley and usually at night

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17
Q

How long does first attack of gout take to resolve if untreated

A

< 2 weeks

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18
Q

In what % of gout does it initally present as polyarticular athritis

A

10

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19
Q

What drug is commonly associated with polyarticular athritis upon first presentation of gout

A

Thiazide diuertic (esp old ladies)

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20
Q

What can happen if gout is left untreated (5)

A
  • Attacks become polyarticular
  • More proximal and upper extremity joints involved
  • Attacks more frequent and last longer
  • Symmetrical, chronic polyarticular athritis
  • Can affect other synovial structures
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21
Q

What are tophi

A

Urate crystals in soft tissue

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22
Q

In what % of untreatedd gout patients to tophi appear

A

50%

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23
Q

When do tophi develop

A

After 10 years

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24
Q

Uric acid is the end stage by product of the metabolism of which molecule

A

Purine

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25
Q

How do humans remove uric acid

A

Via renal excretion and faeces

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26
Q

What value is ‘saturation’ of serum urate

A

6.8mg/dL

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27
Q

What may be develop if excretion is insufficient to maintain serum urate levels below saturation

A

Hyperuricemia

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28
Q

Is over production of urate or under excretion more common in gout

A

Over excretion (90%)

29
Q

Describe the ‘pathway’ of risk factors leading to gout

A
  • Elevated purine sources/ general risk factor lead to increased purines
  • This leads to xanthine
  • This leads to hyperuricemia
  • This leads to reduced renal clearance
30
Q

What are some causes of elevated purine sources

A
  • Catabolism of purines
  • Tumour lysis syndrome
  • Diet
31
Q

What foods are high in purines

A

Beef, pork, lamb, seafood, beer, alcohol

32
Q

Risk factors for gout

A 
Male
Age,
Obesity
Kidney disease
Ethnicity
Polymorphisms
33
Q

What are the risks of hyperuricemia

A 
Joint inflammation
Kidney/ bladder stones
Nephropathy
CV disease
Met. syndromes
34
Q

What can cause decreased renal clearance

A

Drugs like aspirin

Fructose

35
Q

What can cause under-excretion of uric acid

A

Renal insufficiency
Dehydration
Diuretics

36
Q

What must serum levels of urate be higher than for a gout diagnosis

A

5.88mg/dL

37
Q

What score out of 11 is required for a diagnosis of probable gout

A

6

38
Q

What, combined with score, is required to turn diagnosis from probable to definite gout

A

Urate crystals during acute attack

39
Q

What score is required for a diagnosis of ‘not gout’

A

<4

40
Q

What are some differentials of gout

A 
RA
Pseudogout
Psoriatic arthritis
Septic arthritis
Reactive arthritis
41
Q

How is synovial fluid used for a gout diagnosis

A
  • Inflammatory
  • WBC >2000
  • Predominance of polymorphonucleur neutrophils
42
Q

How do urate crystals appear in synovial fluid under polarising light

A

Needle like

High negatively birefringent

43
Q

Is the presence of hyperuricemia diagnostic

A

No

44
Q

Serum uric acid levels above what value should be treated

A

Above 11mg/dL

45
Q

What abnormalities would be seen in a person with gout on x-ray or ultrasound

A
  • Soft tissue swelling
  • Increased blood flow
  • Maintenance of joint space
  • Erosion outside joint capsule. These erosions have overhanging edges called rat bites
46
Q

What does DECT stand for

A

dual energy computed tomography

47
Q

What abnormalities can be detected on a DECT scant

A
  • Uric acid crystal deposits in all late stage patients, and in 60% of early
48
Q

What are the clinical uses of DECT

A
  • Measure MSU volume
  • Changes in actual MSU treatment
  • Predict gout flare
49
Q

What does MSU stand for

A

monosodium urate

50
Q

How do tophaceous deposits lead to bone erosion

A
  • MSU crystals surrounded by granulomatous tissue reaction
  • Produces pro-inflammatory cytokines
  • Stimulates osteoclasts via RANKL
51
Q

What pro-inflammatory cytokines are involved in gout

A

IL1, TNF, IL6

52
Q

4 ways to treat an acute attack of gout

A
  • NSAID
  • Colchicine
  • Coticosteroids
  • IL1 biologicals
53
Q

When should NSAIDS be stopped

A

When symptoms absent for 2 days

54
Q

Why is colchicine second line

A

Narrow theurapeutic window

Toxicity risk

55
Q

Name 3 IL1 biologicals

A

Rilonacept
Canakinumab
Anakinra

56
Q

When are IL1 biologicals used

A

For patients who have severe and frequent flares

57
Q

Name 3 drugs used in the chronic management of gout

A
  • Allopuinol
  • Probenecid
  • Rasburicase
58
Q

How does allopurinol work

A

Blocks xanthine oxidase reducing generation of uric acid

59
Q

How does probenecid work

A

Increases uric acid secretion, fewer significant adverse effects

60
Q

How does rasburicase work

A

Catalyses conversion of uric acid to allantoin

61
Q

What is the proper name for pseudogout

A

Calcium pyrophosphate deposition disease/ chondrocalcinosis

62
Q

What is psudogout

A

The acute deposition of calcium pyrophosphate crystals in and around joints

63
Q

What are the features of pseudo-osteoathritis

A

Osteophytes and soft tissue calcification seen on radiographs

64
Q

What is the underlying pathophysiology of pseudogout (in brief)

A
  • Release of CPPD crystals into joint space
  • Phagocytosis of crystals by monocyte-macrophages or neutrophils
  • Release of cytokines causing inflammation
65
Q

What is the joint most commonly affected by pseudogout

A

Knee

66
Q

What can trigger an acute attack of pseudogout

A

Trauma

Rapid reduction of serum calcium conc.

67
Q

How does synovial fluid appear in pseudogout

A
  • Mild to moderate inflammation

- Rhomboid shaped, weakly birefringent crystals

68
Q

How is pseudogout treated

A

Intra-articular corticosteroids

NSAIDs

LOCO 2 (25 decks)

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