CRYSTAL ARTHRITIS Flashcards
Describe the crystals that form in crystal arthritis
- 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
What is the general pathophysiology of crystal arthritis?
Crystals forming in abnormal sites eg joints,
Gallbladder / kidney( high uric acid)–>elicit local inflammatory response
What are the types of crystal arthritis?
- Gout
- Pseudogout (AKA Pyrophosphate Arthropathy)
What is gout?
-type of crystal arthritis where monosodium urate crystals are deposited in joint lining and elicit an inflammatory response
How is monosodium urate produced?
purines–>uric acid (by xanthin oxidase–>monosodium urate
What serum levels of urate puts patient at risk of gout?
- 0.3mmol / L = Normal
- > 0.36mmol / L = Risk of crystal deposition
- > 0.42mmol/L = supersaturation = deposition very likely
What does a gout attack involve?
Acute inflammation:
-Urate crystals activate phagocytes–>inflammation
What does long term gout lead to?
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
What is pseudogout?
- also called pyrophosphate arthropathy
- calcium pyrophosphate crystals deposited in joint lining–> inflammatory response
- Commonly found by accident from other x rays
What joints are most commonly affected by pseudogout?
Knee > wrist > shoulder > ankle > elbow
What can trigger an acute attack of pseudogout?
- Direct trauma to joint
- Intercurrent illness
- Surgery - esp parathyroidectomy
- Blood transfusion, IV fluid
- T4 replacement
- Joint lavage
- Most are spontaneous
What are the risk factors of crystal arthritis?
- 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)
Describe hyperuricemia
- excess uric acid
- affects up to 10% of the population
- major RF for gout
- Usually due to under excretion(renal problems)
What can cause hyperuricemia due to under excretion of uric acid?
- Alcohol
- renal impairment
- hypertension
- inherited
- hypothyroid/hyperPTH
- Obesity
- DM
- Drugs
What can cause hyperuricemia due to overproduction of uric acid?
- Diet; alcohol, excess meet/shellfish/offal, yeast extract
- hyperlipidaemia
- myoproliferative disease
- cytotoxic drugs
- psoriasis
- Lesch-Nyhan Syndrome
What drugs can lead to hyperuricemia?
- Low dose aspirin
- Diuretics (esp thiazides)
- Cyclosporin / tacrolimus
- Ethambutol / pyrazinamide
- Lead poisoning
Describe the presentation of gout
- 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
Describe the presentation of pseudogout
- Normally monoarthritis, polyarticular rare
- Severe pain
- Stiffness
- Swelling
- Fever
- Resolution in 1-3 weeks
What are the investigations for gout and pseudogout?
- 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
What might an X-ray show in gout?
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)
What might an X-ray show in pseudogout?
Chondrocalcinosis - linear calcification parallel to articular surfaces (can help distinguish from OA)
What would microscopy of Synovial Fluid show in gout?
Negative birefringent needles
What would microscopy of Synovial Fluid show in psuedogout?
Positively birefringent rhomboids
What is the acute treatment for gout?
- NSAIDs (eg diclofenac) or coxibs (eg lumiracoxib)
- Colchicine ONLY if NSAIDs are not tolerated
- Corticosteroids (IM or intra-articular depot -methylprednisolone)
What is the long term treatment for gout?
- 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
What are the side effects of allopurinol?
- 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
What is the treatment for pseudogout?
- 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.
