Crystal Arthropathies Flashcards

1
Q

Define gout

A

Disorder of uric acid metabolism leading to monosodium urate crystal deposition in the joints, soft tissues and kidneys, causing recurrent bouts of acute arthritis.

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2
Q

Aetiology of gout

A

Underlying metabolic disturbance is hyperuricaemia, which may be caused by:
→ Increased urate intake or production (10%): Increased dietary intake, increased purine turnover (lymphoma, leukaemia, polycythaemia vera, psoriasis), increased synthesis in Lesch-Nyhan syndrome**
→ Decreased renal excretion (90%): Idiopathic, drugs*, renal dysfunction

*CANT LEAP (Ciclosporin, alcohol, nicotinic acid, thiazides, loop diuretics, ethambutol, aspirin, pyrizanamide
**Lesch–Nyhan syndrome (gout + mental retardation + self- mutilating behaviour)

Acute (Podagra) or chronic (Tophaceous)

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3
Q

Risk factors for gout

A

Dietary factors (seafood, meat and alcohol (esp. beer) consumption
Older age
Male sex
Menopausal
Drugs (CANT LEAP)
Obesity (adiposity)
Insulin resistance
Hypertension
Renal insufficiency
Hyperlipidaemia
Family history

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4
Q

Symptoms of gout

A

Episodes of pain (acute attack)
- Rapid onset
- Severe/excruciating
- Monoarticular
- Commonly the first metatarsophalangeal joint
- Peak at 24 hours, resolve in 7-10 days
- Precipitated by trauma, infection, alcohol, introduction or withdrawal of hypouricaemic agents
- Asymptomatic between acute attacks (intercritical gout)
Joint stiffness
Swelling
Tenderness
Chronic tophaceous gout: follow repeated acute attacks - persistent low-grade fever, polyarticular pain with painful tophi on the tendons and pinna of ear
Symptoms of urate urolithiasis (kidney involvement)

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5
Q

Signs of gout on examination

A

Tophi
Joint stiffness
Foot joint distribution
Swelling and join effusion
Erythema and warmth

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6
Q

Investigations for gout

A

Bloods only, further Ix in secondary care if uncertain or unconfirmed

Uric acid: raised >416 (M) or >360 (F), usually 2 weeks after an attack
FBC: Raised WCC
ESR: raised
Renal screen: ?CKD

Arthrocentesis with synovial fluid analysis: raised WCC, negatively birefringent needle-shaped crystals under polarised light with red filter (blue needles, left→ right)
MC&S synovial fluid: negative
US: erosions, tophi, double contour line
X-ray affected joint: peri-articular lesions, ‘rate bite’ erosions

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7
Q

Management for acute gout attacks

A
  1. NSAIDs e.g. naproxen 500mgs bd (do not give if CKD is the cause of gout)
  2. Colchicine 500mcg 2x a day (inhibit microtubule assembly in neutrophils by inhibiting tuberculin)
  3. Glucocorticoids e.g. prednisolone 15-20mgs for 7 days / intra-articular steroids

All 3 contraindicated → IL-1 inhibitor

+ Advice:
- Apply ice packs to the joint
- Use paracetamol
- Education on gout
- Rest and elevate
- Keep joint exposed and in a cool environment
- Return if symptoms get worse or there is not improvement after 1-2 days

Follow-up in 4-6 weeks and check BP, HbA1c, serum urate, U&Es, lipids → consider ULT

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8
Q

Management between attacks for gout

A

Conservative
- Hydrate
- Reduce purine intake: anchovies, sardines, mackerel, offal, game
- Moderate spinach, cauliflower, asparagus, mushrooms, lentils/peas/beans, meat, fish
- Avoid alcohol
- Avoid prolonged fasting

Medical: urate lowering therapy
- Allopurinol (reduce synthesis; ok in CKD, Does not need to be stopped if already established), Febuxostat
- Probenecid (increase urate excretion; only give if GFR >50), losartan
- Recombinant urate oxidase: rasburicase

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9
Q

Complications of gout

A

Chronic arthritis if untreated (2%)
Joint damage
Reduced QOL
Renal stones
Tophi -> inflammation, exudative, secondary infection
Cardiovascular disease and mortality
Ass. With CKD

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10
Q

Prognosis for gout

A

Acute attacks are self-limiting, if untreated with resolve spontaneously over 5-15 days (+ pruritus and desquamation of overlying skin)
Risk of recurrence is 62% without urate lowering therapies (ULT) in the first year, 78% in the second and 84% in the third year
Treatment can suppress attacks and recurrence

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11
Q

What is pseudogout

A

arthritis associated with deposition of calcium pyrophosphate dihydrate (CPPD) crystals in joint cartilage

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12
Q

What is the aetiology and risk factors of pseudogout

A

May be predisposed by osteoarthritis, trauma, haemochromatosis, hyperparathyroidism, hypomagnesaemia, hypophosphatasia

CPPD crystals formed in cartilage near chondrocyte surface → excessive production and deposition → sheds into joint cavity → arthritis

RF:
- older age
- injury
- hyperPTH
- haemochromatosis
- HypoMg/PO4

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13
Q

Symptoms and signs of pseudogout

A

Painful and tender joints
- Acute - larger joints: painful, swollen knee, ankle, shoulder, elbow, wrist
- Chronic: pain, stiffness, functional impairment
Sudden worsening of osteoarthritis
Red and swollen joints
Fever and malaise
Tendonitis, tenosynovitis, bursitis (rare)

Acute arthritis: Red, hot, tender, restricted range of movement, fever
Chronic arthropathy: bony swelling, crepitus, deformity, restriction of movement

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14
Q

Investigations for pseudo gout

A

Bone profile: raised Ca, PTH deranged
U&Es: hypoMg/PO4
FBC: raised WCC
ESR: raised

Arthrocentesis with synovial fluid analysis: pyrophosphate rhomboid crystals positive birefringence under polarised light
X-ray affected joint: linear, stippled radio-opaque deposits in the fibro-cartilate/hyaline articular cartilage + osteoarthritic changes (LOSS)

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15
Q

Management for pseudogout

A

Analgesia
NSAIDs
PO/IM/intra-articular steroids
Colchicine
Symptomatic relief: cool pacts, temporary rest

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