Ankylosing Spondylitis & Gouts Flashcards

1
Q

What is Ankylosing Spondylitis?

A
  • Ankylosing spondylitis is a HLA-B27 associated spondyloarthropathy.
  • It typically presents in males (sex ratio 3:1) aged 20-30 years old
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2
Q

What are features of Ankylosing Spondylitis?

A
  • Typically a young man who presents with lower back pain and stiffness of insidious onset
  • Stiffness is usually worse in the morning and improves with exercise
  • Patient may experience pain at night which improves on getting up
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3
Q

What are examination findings of Ankylosing Spndylitis?

A
  • Reduced lateral flexion
  • Reduced forward flexion
    • Schober’s test - a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible
  • Reduced chest expansion
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4
Q

What are extra-articular features of Ankylosing Spondylitis?

A
  • Apical fibrosis
  • Anterior uveitis
  • Aortic regurgitation
  • Achilles tendonitis
  • AV node block
  • Amyloidosis
  • and cauda equina syndrome
  • peripheral arthritis (25%, more common if female)
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5
Q

What are blood tests and typical result in Ankylosing spondylitis?

A
  • CRP and ESR may be elevated but can be normal. This does not exclude ankylosing spondylitis
  • HLA-B27 is of little use in making the diagnosis as it is positive in:
    • 90% of patients with ankylosing spondylitis
    • 10% of normal patients
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6
Q

What are radiological investigations in Ankylosing Spondylitis?

A
  • MRI of the spine and Sacroiliac joints is more sensitive for early disease
  • X-ray of the sacroiliac joints and spine is the most useful investigation in establishing the diagnosis in later disease.
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7
Q

What are the changes seen on X-Ray for Ankylosing Spondylitis?

A

Radiographs may be normal early in disease, later changes include:

  • Sacroiliitis: subchondral erosions, sclerosis
  • Squaring of lumbar vertebrae
  • ‘Bamboo spine’ (late & uncommon)
  • Romanus lesions
  • Syndesmophytes: due to ossification of outer fibres of annulus fibrosus
  • Chest x-ray: apical fibrosis
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8
Q

What other investigations can be performed to assess effects of Ankylosing Spondylitis?

A

Spirometry may show a restrictive defect due to a combination:

  • Pulmonary fibrosis
  • Kyphosis
  • Ankylosis of the costovertebral joints.
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9
Q

How is Ankylosing Spondylitis managed?

A
  • Encourage regular exercise such as swimming
  • Physiotherapy
  • NSAIDs are the first-line treatment
  • The disease-modifying drugs which are used to treat rheumatoid arthritis (such as sulphasalazine) are only really useful if there is peripheral joint involvement
    • TNF inhibitor, IL-17 inhibitors if DMARDs fail
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10
Q

What is Gout?

A
  • Form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium.
  • It is caused by chronic hyperuricaemia (uric acid > 0.45 mmol/l)
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11
Q

What are caauses of Gout?

A
  • Decreased excretion of uric acid
    • drugs*: diuretics
    • chronic kidney disease
    • lead toxicity
  • Increased production of uric acid
    • Myeloproliferative/lymphoproliferative disorder
    • Cytotoxic drugs
    • Severe psoriasis
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12
Q

What can Gout lead to ?

A
  • Acute and chronic arthritis
  • Soft tissue masses called tophi
  • Urate nephropathy
  • Uric acid nephrolithiasis.
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13
Q

What are investigations done for diagnosis of Gout?

A
  • Urate levels
  • Monosodium Urate crystals found in synovial fluid aspirate are pathognomonic for gout
    • Urate crystals are negatively birefringent through polarised light.
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14
Q

What are some risk factors for Gout?

A
  • Non-modifiable factors
    • Age >40 years
    • Male gender
  • Modifiable factors
    • Increased purine uptake (meats and seafood) Alcohol intake (especially beer)
    • High fructose intake
    • Obesity
    • Congestive heart failure
    • Coronary artery disease
    • Dyslipidemia
    • Renal disease
    • Organ transplant
    • Hypertension
    • Smoking
    • Diabetes mellitus
    • Urate-elevating medications e.g. diuretics
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15
Q

How can Gout be prevented?

A
  • Maintain optimal weight
  • Regular exercise
  • Diet modification (purine-rich foods)
  • Reduce alcohol consumption (beer and liquor)
  • Smoking cessation
  • Maintain fluid intake and avoid dehydration
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16
Q

What is the acute management of Gout?

A
  • 1st line: NSAIDs or Colchicine
    • Gastroprotection may also be indicated
    • Colchicine* has a slower onset of action. The main side-effect is diarrhoea
  • Oral steroids may be considered if NSAIDs and colchicine are contraindicated.
    • A dose of prednisolone 15mg/day is usually used
    • Another option is intra-articular steroid injection
  • if the patient is already taking allopurinol it should be continued
17
Q

What are indications for urate-lowering therapy (ULT)?

A
  • All patients after their first attack of gout
  • ULT is particularly recommended if:
    • >= 2 attacks in 12 month
    • Tophi
    • Renal disease
    • Rric acid renal stones
    • Prophylaxis if on cytotoxic or diuretics
18
Q

What are Urate Lowering Therapy?

A
  • 1st Line: Allopurinol (febuxostat can be used instead if not tolerated)
    • Initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 300 µmol/l. Lower initial doses should be given if the patient has a reduced eGFR
    • Xanthine oxidase inhibitors (both)
    • colchicine cover should be considered when starting allopurinol.
  • Benzbromarone and sulfinpyrazone are used less commonly as more side effects. They act to increase renal excretion of uric acid.
    • Aim to reduce SUA to < 360micromol/L
19
Q

What other medications can be considered in patients with Gout?

A
  • Losartan has a specific uricosuric action and may be particularly suitable for the many patients who have coexistent hypertension
  • Increased vitamin C intake (either supplements or through normal diet) may also decrease serum uric acid levels
20
Q

What is Psoriatic Arthropathy?

A
  • Psoriatic arthropathy correlates poorly with cutaneous psoriasis and often precedes the development of skin lesions.
  • Around 10-20% percent of patients with skin lesions develop an arthropathy with males and females being equally affected
21
Q

What are examination findings of Psoriatic Arthropathy?

A
  • Oligo-arthritis with dactylitis or sausage digit
  • Can be symmetrical arthritis.
  • Severe deformities (arthritis mutilans)
22
Q

What are investigations for Psoriatic Arthropathy?

A
  • CRP often raised
  • Central joint erosion seen early on ultrasound or MRI leading to ‘pencil in cup’ x-ray appearance
23
Q

What is the management of Psoriatic Arthropathy?

A
  • Treat as rheumatoid arthritis but better prognosis
  • NSAIDs, DMARDs, TNF inhibitors, IL-17 inhibitors, IL12/23 inhibitors.
24
Q

What is Pseudogout?

A

Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate in the synovium

25
Q

What are Risk Factors for Pseudogout?

A
  • Hyperparathyroidism
  • Hypothyroidism
  • Haemochromatosis
  • Acromegaly
  • Low magnesium
  • Low phosphate
  • Wilson’s disease
26
Q

What are features of Pseudogout?

A
  • Knee, wrist and shoulders most commonly affected
  • Joint aspiration: weakly-positively birefringent rhomboid shaped crystals
  • X-Ray: chondrocalcinosis
27
Q

How is Pseudogout managed?

A
  • Aspiration of joint fluid, to exclude septic arthritis
  • NSAIDs or intra-articular, intra-muscular or oral steroids as for gout