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Z Year 2 BRS MSK > Introduction to Rheumatology 2 > Flashcards

Introduction to Rheumatology 2 Flashcards

1
Q

What is extensor tensosynovitis?

A
  • swelling is not above either the wrist or MCP joints
  • incomplete extension of the little and ring fingers (cannot stick the fingers out straight) – this is consistent with extensor tendon damage by the tenosynovitis
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2
Q

What are the common extra-articular features of RA?

A
  1. Fever, weight loss

2. Subcutaneous nodules

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3
Q

What are the uncommon extra-articular features of RA?

A
  1. vasculitis
  2. Ocular inflammation e.g. episcleritis
  3. Neuropathies
  4. Amyloidosis
  5. Lung disease – nodules, fibrosis, pleuritis
  6. Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis
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4
Q

What is subcutaneous nodules in RA?

A

central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue

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5
Q

How common are subcutaneous nodules in RA?

A

around 30% of patients

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6
Q

What are subcutanous nodules in RA associated with?

A
  1. Severe disease
  2. Extra-articular manifestations
  3. Rheumatoid factor
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7
Q

What are rheumatoid nodules in the hands?

A
  • common location and not easily missed

- can see them around the PIP joint of the right index and left index, middle and ring fingers

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8
Q

Where is a common rheumatoid nodules?

A

(1. ulnar border of forearm) where you might detect nodules
2. if present it confirms the diagnosis of rheumatoid arthritis and is invariably associated with rheumatoid factor
3. Do not forget to examine this area carefully in patients with polyarthritis – it would be foolish to miss such an important clinical finding

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9
Q

What are the two types of antibodies found in the blood of RA patients?

A
  1. Rheumatoid factor

2. Antibodies to citrullinated protein antigens (ACPA)

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10
Q

What is Rheumatoid factor?

A

Antibodies that recognize the Fc portion of IgG as their target antigen

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11
Q

What type of antibodies are in rheumatoid factor?

A

IgM antibodies i.e. IgM anti-IgG antibody !

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12
Q

When is rheumatoid factor positive?

A

positive in 70% at disease onset and further 10-15% become positive over the first 2 years of diagnosis

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13
Q

What are ACPA?

A
  • highly specific for rheumatoid arthritis

- Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’

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14
Q

What is the citrullination of peptides mediated by?

A

enzymes called Peptidyl arginine deiminases (PADs)

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15
Q

What is the treatment goal in RA management?

A

prevent joint damage

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16
Q

What is required to prevent joint damage in RA?

A
  1. Early recognition of symptoms, referral and diagnosis
  2. Prompt initiation of treatment: joint destruction = inflammation x time
  3. Aggressive treatment to suppress inflammation
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17
Q

What class of drugs are used in RA?

A

Disease-modifying anti-rheumatic drugs (‘DMARDs’) = drugs that control the disease process

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18
Q

What is the 1st line drug treatment for RA?

A

methotrexate in combination with hydroxychloroquine or sulfasalazine

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19
Q

What is the 2nd line drug treatment in RA?

A

Biological therapies offer potent and targeted treatment strategies
New therapies include Janus Kinase inhibitors : Tofacitinib & Baricitinib

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20
Q

What other therapies are

useful in RA treatment?

A
  1. Important roles for glucocorticoid therapy (prednisolone) but avoid long-term use because of side-effects.
  2. Multidisciplinary approach also important e.g. physiotherapy, occupational therapy, hydrotherapy, surgery
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21
Q

What are biological therapies?

A

proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine

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22
Q

What biological therapies are used in RA?

A
  1. Inhibition of tumour necrosis factor alpha (anti-TNF)
  2. b cell depletion
  3. Modulation of T cell co-stimulation
  4. Inhibition of Il-6 signalling
23
Q

What are examples of anti-TNF?

A
  1. antibodies (infliximab, and others)

2. fusion proteins (etanercept)

24
Q

What are examples of b cell depletion biological therapies?

A

Rituximab – antibody against the B cell antigen, CD20

25
Q

What are examples of modulation of T Cell co stimulation biological therapies?

A

Abatacept - fusion protein - extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to modified Fc (hinge, CH2, and CH3 domains) of human immunoglobulin G1

26
Q

What are examples of inhibition of Il-6 signalling biological therapies?

A
  1. Tocilizumab (RoActemra) – antibody against interleukin-6 receptor.
  2. Sarilumab (Kevzara) – antibody against interleukin-6 receptor.
27
Q

What is ankylosing spondylitis?

A
  • Common demographic: 20-30yrs, M

* Associated with HLA B27

28
Q

When happens in ankylosing spondylitis (AS)?

A
  1. Seronegative spondyloarthropathy – no positive autoantibodies
  2. Chronic sacroillitis – inflammation of sacroiliac joints
  3. Results in spinal fusion – ankylosis
29
Q

What is the clinical presentation of AS?

A
  1. Lower back pain + stiffness
    - Early morning
    - Improves with exercise
  2. Reduced spinal movements
  3. Peripheral arthritis
  4. Plantar Fasciitis, Achilles Tendonitis
  5. Fatigue
30
Q

What blood tests are done in the investigation of AS?

A
  1. Normocytic anaemia
  2. Raised CRP, ESR
  3. HLA-B27
31
Q

What imaging and findings are in AS?

A
  1. X-Ray
  2. MRI
    - Squaring Vertebral bodies, Romanus lesion
    - Erosion, sclerosis, narrowing SIJ
    - Bamboo Spine
    - Bone Marrow Oedema
32
Q

What is the management of AS?

A
  • Physiotherapy
  • Exercise regimes
  • NSAIDs
  • Peripheral joint disease - DMARDs
33
Q

What is psoriatic arthritis?

A

autoimmune disease affecting the skin (scaly red plaques on extensor surfaces eg elbows and knees)

34
Q

How common is joint inflammation in psoriasis?

A

10%

35
Q

Are rheumatoid factors present in psoriatic arthritis?

A

NO

36
Q

What is clinical presentation of psoriatic arthritis?

A

asymmetrical arthritis affecting IPJs

37
Q

How else can psoriatic arthritis manifest?

A

1, Symmetrical involvement of small joints (rheumatoid pattern)

  1. Spinal and sacroiliac joint inflammation
  2. Oligoarthritis of large joints
  3. Arthritis mutilans
38
Q

What are the investigations and findings in psoriatic arthritis?

A
  1. X-rays of affected joints – pencil in cup abnormality
  2. MRI – sacroiliitis and enthesitis
  3. Bloods – no antibodies as seronegative
39
Q

What is the management of psoriatic arthritis?

A
  1. DMARDs – methotrexate

2. Avoid oral steroids – risk of pustular psoriasis due to skin lesions

40
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection especially urogenital (e.g. Chlamydia trachomatis) and gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections) infections

41
Q

What are the other important extra-articular manifestations of reactive arthritis?

A
  1. Enthesitis (tendon inflammation)
  2. Skin inflammation
  3. Eye inflammation
42
Q

What may reactive arthritis be a first manifestation of?

A

HIV or Hep C

43
Q

When can people get reactive arthritis?

A

young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection)

44
Q

How long does reactive arthritis last?

A
  • Symptoms follow 1-4 weeks after infection and this infection may be mild
  • Condition is usually self-limiting – can be managed with NSAIDS or DMARDs if required
45
Q

What is reactive arthritis distinct from?

A

infection in joints (septic arthritis)

46
Q

What is lupus?

A

a multi-system autoimmune disease

47
Q

What can SLE affect?

A
  1. Multi-site inflammation: can affect any almost any organ.

2. Often joints, skin, kidneys, haematology and lungs, CNS involvement

48
Q

What is SLE assoicated with?

A
  1. Associated with antibodies to self antigens (‘autoantibodies’)
  2. Autoantibodies are directed against components of the cell nucleus (nucleic acids and proteins)
49
Q

What clinical tests are used in SLE?

A
  1. Antinuclear antibodies (ANA)

2. Anti-double stranded DNA antibodies (anti-dsDNA Abs)

50
Q

What does ANA look at?

A
  1. High sensitivity for SLE but not specific.

2. A negative test rules out SLE, but a positive test does not mean SLE

51
Q

What does anti-dsDNA Abs look at?

A

High specificity for SLE in the context of the appropriate clinical signs

52
Q

What is the epidemiology of SLE?

A
  • F:M ratio 9:1
  • Presentation 15 - 40 yrs
  • Increased prevalence in African and Asian ancestry populations
  • Prevalence varies 4-280/100,000
53
Q

What are other CTDs?

A
  • Systemic Sclerosis
  • Myositis
  • Sjogrens syndrome
  • Mixed connective tissue disease

Z Year 2 BRS MSK (18 decks)

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