MSK Flashcards

1
Q

What investigations are suggestive of a diagnosis of gout?

A
  • Serum urate level >360 micromol/L (can be normal)
  • Joint aspiration → needle-shaped monosodium urate crystals with negative birefringence confirms diagnosis
  • X-ray of affected joint → if uncertain diagnosis
    • Maintained joint space, lytic lesions in the bone, punched out erosions which can have sclerotic borders with overhanging edges.
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2
Q

How is an acute flare of gout managed?

A
  • 1st line → NSAIDs (co-prescribed with PPI cover). Naproxen 500mg BD
  • 2nd line → colchicine 500mg BD
    • Useful if NSAIDs contraindicated
    • Abdominal symptoms & diarrhoea are common side effects
  • 3rd line → oral steroids. Prednisolone 30mg OD 7 days
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3
Q

What medications can be started for gout prophylaxis? When should they be started, what is the target urate levels & what happens when there is an acute flare?

A
  • 1st line → allopurinol, aiming for urate level <300
  • 2nd line → febuxostat

Start >2 weeks after an acute flare. Continue allopurinol during any future gout flares.

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4
Q

How does polymyalgia rheumatica present?

A
  • Symptom onset days-weeks → must be present for 2 weeks before a diagnosis is considered.
  • Pain & stiffness of:
    • Shoulders → can radiate to the upper arm & elbow
    • Pelvic girdle → around hips & radiating to thighs
    • Neck
  • Symptoms are worse in the morning & take >45mins to improve, after rest/inactivity, and interfere with sleep.
  • Associated features:
    • Systemic symptoms → weight loss, fatigue, low-grade fever
    • Muscle tenderness
    • Carpal tunnel syndrome
    • Peripheral oedema
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5
Q

How is polymyalgia rheumatica managed?

A
  • Low-dose corticosteroids
    • 15mg prednisolone & follow-up in 1 week. Patients notice a dramatic improvement in symptoms within 1 week → if not, then consider an alternative diagnosis.
    • Typically on steroids for 1-2 years, with the steroids being gradually reduced.
  • Vitamin D & calcium supplementation, consider bisphosphonates → due to steroid-related osteoporosis risk.
  • Consider PPIs for gastro-protection
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6
Q

What is fibromyalgia & how does it present?

A

= a chronic widespread pain disorder of unknown origin.
- Widespread pain → constant, dull ache
- Low back pain with/without radiation to the bum & legs
- Neck pain & across the shoulders
- Fatigue, unrefreshing sleep
- Sleep disturbance
- Morning stiffness
- Mood disorders → depression & anxiety
- Cognitive problems → focus, memory, word-finding difficulties
- Headaches

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7
Q

What is ankylosing spondylitis, and how does it present?

A

= a seronegative, chronic inflammatory arthritis affecting the axial skeleton (spine & sacroiliac joints).
- Typically a male in their 20’s, with symptoms developing gradually over 3 months.
- Inflammatory back pain
- Pain & stiffness in lower back, worse in the morning & at night, improves with activity.
- Sacroiliac pain
- Large joint arthritis
- Extra-articular involvement:
- Anterior uveitis
- Aortic regurgitation
- IgA nephropathy
- Upper lobe fibrosis
- Inflamed costosternal & costovertebral joints → chest pain & SOB due to restricted movement.
- imited ROM of back in all directions
- Abnormal Schober’s Test
- Reduced chest expansion

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8
Q

What gene is present in 90% of people with ankylosing spondylitis?

A

90% of patients with AS will have the HLA-B27 gene, so this can be tested for in secondary care to support a diagnosis.

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9
Q

How does ankylosing spondylitis look on an x-ray?

A
  • Sacroiliitis, or fusion of the joint in more advanced disease
  • Squared vertebral bodies
  • In late disease → bamboo spine, due to complete fusion of the vertebral spine
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10
Q

How is ankylosing spondylitis managed?

A
  • PA & physiotherapy → to improve & maintain posture, flexibility & mobility.
  • Pharmacological:
    • 1st line → NSAIDs (with PPI). Trial of at least 2 for 2-4 weeks before moving to 2nd line.
    • 2nd line → Biologics, anti-TNF such as infliximab
    • If peripheral joint disease → DMARDs, such as sulfasalazine & methotrexate, but these are not effective for axial disease
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11
Q

What are the common joints in the hand which are affected in rheumatoid arthritis?

A

MCP, PIP, wrist

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12
Q

How is rheumatoid arthritis managed initially or during an acute flare?

A
  • Short-term steroids → oral or IM, for shortest possible period, at lowest possible dose.
  • NSAIDs (with PPI) → for analgesic benefit
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13
Q

What are the side-effects of methotrexate?

A
  • Mouth ulcers & mucositis
  • Liver toxicity
  • Bone marrow suppression & leukopenia
  • Teratogenic
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14
Q

What are the 2 common triggers of reactive arthritis?

A
  • Gastroenteritis
  • STIs → chlamydia. Gonorrhoea will typically cause septic arthritis rather than RA.
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15
Q

How does compartment syndrome present?

A
  • Pain → Disproportionate pain, severe, medications do very little. Worsened by passive stretching of muscles. Increasing with time
  • Paraesthesia
  • Tense on palpation, difficult to mobilise.
  • Will still have a pulse, differentiating this from acute limb ischaemia
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16
Q

What is Systemic Lupus Erythematous & how does it present?

A

= a complex multisystem inflammatory autoimmune connective tissue disease, which has variable clinical manifestations among different patients.

Generally presents with non-specific symptoms:

  • Constitutional symptoms:
    • Fatigue → common
    • Weight loss
    • Fever
    • Myalgia
    • Lymphadenopathy
  • Arthralgia & non-erosive arthritis → can be one of the earliest presentations
  • Photosensitive malar rash, discoid rash
  • Raynaud’s phenomenon
  • Hair loss
  • Mouth ulcers
  • Pleuritic chest pain
  • Shortness of breath
17
Q

What are the two common antibodies tested for in suspected SLE?

A
  • Antinuclear Antibody (ANA) → present in 5% of healthy people, and >95% of people with SLE.
  • Anti-double stranded DNA (Anti-dsDNA) → highly specific to SLE, but only around 70% of patients with SLE will have them.
18
Q

What medications are prescribed for SLE?

A
  • Mild → hydroxychloroquine (prevents disease progression), NSAIDs, can add in corticosteroids for flares.
  • Moderate/treatment-resistant → DMARDs, biologics
19
Q

What is sarcoidosis? Who is most likely to develop it?

A

= a chronic granulomatous, multi-system disorder.

  • Granulomas are inflammatory nodules full of macrophages, the cause of which is unknown.
    More common in women, aged 20-40yr olds, people of black ethnic origin.
20
Q

What are the two key blood tests which are abnormal with sarcoidosis?

A
  • Raised calcium
  • Raised angiotensin-converting enzyme
21
Q

If treatment is required, how is sarcoidosis managed?

A
  • Oral steroids (6-24 months) are usually 1st-line where treatment is required. Bisphosphonate cover required.
  • Methotrexate 2nd line
22
Q

How does osteomalacia present?

A
  • Fatigue
  • Pain in the lower back, hips, and pelvis
  • Muscle weakness
  • Bone tenderness
  • Pseudofractures/Looser’s zones → areas of incomplete stress fractures
23
Q
A