CRYSTAL ARTHRITIS Flashcards

1
Q

Describe the crystals that form in crystal arthritis

A
  • Homogenous solid
  • Ions bonded closely in ordered repeating symmetric arrangement
  • Stable, hard, high density
  • Strengthens endo and exo skeleton
  • Remove excess ions (surface binding)
  • Can be made from urate, calcium pyrophosphate of hydroxyapatite
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2
Q

What is the general pathophysiology of crystal arthritis?

A

Crystals forming in abnormal sites eg joints,

Gallbladder / kidney( high uric acid)–>elicit local inflammatory response

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3
Q

What are the types of crystal arthritis?

A
  • Gout

- Pseudogout (AKA Pyrophosphate Arthropathy)

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4
Q

What is gout?

A

-type of crystal arthritis where monosodium urate crystals are deposited in joint lining and elicit an inflammatory response

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5
Q

How is monosodium urate produced?

A

purines–>uric acid (by xanthin oxidase–>monosodium urate

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6
Q

What serum levels of urate puts patient at risk of gout?

A
  • 0.3mmol / L = Normal
  • > 0.36mmol / L = Risk of crystal deposition
  • > 0.42mmol/L = supersaturation = deposition very likely
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7
Q

What does a gout attack involve?

A

Acute inflammation:

-Urate crystals activate phagocytes–>inflammation

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8
Q

What does long term gout lead to?

A

tophaceous gout

  • Onion like aggregates of urate crystals with inflammatory cells-tophi
  • 6-9 months to control attacks
  • Up to 2 years for tophi to resolve
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9
Q

What is pseudogout?

A
  • also called pyrophosphate arthropathy
  • calcium pyrophosphate crystals deposited in joint lining–> inflammatory response
  • Commonly found by accident from other x rays
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10
Q

What joints are most commonly affected by pseudogout?

A

Knee > wrist > shoulder > ankle > elbow

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11
Q

What can trigger an acute attack of pseudogout?

A
  • Direct trauma to joint
  • Intercurrent illness
  • Surgery - esp parathyroidectomy
  • Blood transfusion, IV fluid
  • T4 replacement
  • Joint lavage
  • Most are spontaneous
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12
Q

What are the risk factors of crystal arthritis?

A
  • Gender: Females more common
  • Age: Common over 40 years, <30 year is uncommon
  • Family history
  • Existing metabolic disease
  • Existing comorbidities (CVD, hypertension, DM, chronic renal failure)
  • Hyperuricemia
  • Treatment for other conditions(NSAIDs, anti-inflammatories, colchicine, steroids, diuretics)
  • Existing crystals = faster growth of bigger crystals (amplification loop hypothesis)
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13
Q

Describe hyperuricemia

A
  • excess uric acid
  • affects up to 10% of the population
  • major RF for gout
  • Usually due to under excretion(renal problems)
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14
Q

What can cause hyperuricemia due to under excretion of uric acid?

A
  • Alcohol
  • renal impairment
  • hypertension
  • inherited
  • hypothyroid/hyperPTH
  • Obesity
  • DM
  • Drugs
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15
Q

What can cause hyperuricemia due to overproduction of uric acid?

A
  • Diet; alcohol, excess meet/shellfish/offal, yeast extract
  • hyperlipidaemia
  • myoproliferative disease
  • cytotoxic drugs
  • psoriasis
  • Lesch-Nyhan Syndrome
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16
Q

What drugs can lead to hyperuricemia?

A
  • Low dose aspirin
  • Diuretics (esp thiazides)
  • Cyclosporin / tacrolimus
  • Ethambutol / pyrazinamide
  • Lead poisoning
17
Q

Describe the presentation of gout

A
  • Hot Swollen joints
  • Shiny red and taut
  • Common joints: ankle, foot, small joints of hand, wrist, elbow or knee
  • Pain (no more connective tissue, just bone on bone)
  • May be polyarticular, but typically monoarticular
18
Q

Describe the presentation of pseudogout

A
  • Normally monoarthritis, polyarticular rare
  • Severe pain
  • Stiffness
  • Swelling
  • Fever
  • Resolution in 1-3 weeks
19
Q

What are the investigations for gout and pseudogout?

A
  • X-ray
  • Aspirate joint–>polarized light Microscopy of Synovial Fluid
  • U&E for gout; serum uric acid and urea/creatinine to check for renal impairment
  • FBC for pseudogout- may show raised WCC
20
Q

What might an X-ray show in gout?

A

B - Bony hooks (from erosions)
E - Erosions (punched out)
T - tophi (soft tissue masses) - more opaque (replaced by crystals)
S - Space intact (no loss of joint space)

21
Q

What might an X-ray show in pseudogout?

A

Chondrocalcinosis - linear calcification parallel to articular surfaces (can help distinguish from OA)

22
Q

What would microscopy of Synovial Fluid show in gout?

A

Negative birefringent needles

23
Q

What would microscopy of Synovial Fluid show in psuedogout?

A

Positively birefringent rhomboids

24
Q

What is the acute treatment for gout?

A
  • NSAIDs (eg diclofenac) or coxibs (eg lumiracoxib)
  • Colchicine ONLY if NSAIDs are not tolerated
  • Corticosteroids (IM or intra-articular depot -methylprednisolone)
25
Q

What is the long term treatment for gout?

A
  • Aim: Urate < 0.3mmol / L
  • Non pharma: lose weight, reduce alcohol / shellfish, avoid purine rich foods
  • Withdraw drugs such as thiazides and salicylates
  • Xanthine Oxidase Inhibitors for those with frequent attacks, eg Allopurinol
  • Cover with colchicine 0.5mmg OD or BD for 6 months or NSAIDs for 6 weeks to prevent acute attack
26
Q

What are the side effects of allopurinol?

A
  • Do not start within 1 month after acute attack (as it might induce another acute attack)
  • 2% will get rash, headache, myalgia
  • Very rare hypersensitivity syndrome
  • Watch renal function
27
Q

What is the treatment for pseudogout?

A
  • Pathology not really known, so there aren’t that many good treatments
  • Advise to reduce food with high purine content.
  • Use of cool packs in acute attack, rest.
  • Methotrexate and hydroxychloroquine may be considered for chronic pseudogout.