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Year 3 MSK > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is rheumatology?

A

The medical specialty dealing with diseases of the musculoskeletal system

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2
Q

What are the components of synovial joints?

A

Two bones forming the join

Joint cavity with synovial fluid and cartilage on either side (type II cartilage)

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3
Q

What is Arthritis?

A

Disease of the joints

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4
Q

What are the 2 types of arthritis?

A 
Osteoarthritis
Inflammatory arthritis (rheumatoid)
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5
Q

What is inflammation?

A

a physiological response to deal with injury or infection

However, excessive/inappropriate inflammatory reactions can damage the host tissues

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6
Q

How does inflammation clinically manifest?

A 
Rubor
Dolor
Calor
Tumor
Loss of function
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7
Q

What are the physiological changes associated with inflammation?

A
  • Increased blood flow
    -Migration of white blood cells (leucocytes) into the tissues
    -Activation/differentiation of leucocytes
    -Cytokine production
    E.g. TNF-alpha, IL1, IL6, IL17
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8
Q

What are the two types of crystal arthritis?

A

Gout

Pseudogout

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9
Q

What is gout caused by?

A

syndrome caused by deposition of urate (uric acid) crystals -> inflammation

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10
Q

What is a risk factor for gout?

A

High uric acid levels (hyperuricaemia)

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11
Q

What causes hyperuricaemia?

A 
Genetic tendency
Increased intake of purine rich foods
Reduced excretion (kidney failure)
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12
Q

What is pseudogout caused by?

A

a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals -> inflammation

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13
Q

What are the risk factors for pseudogout?

A

background osteoarthritis, elderly patients, intercurrent infection

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14
Q

What does gout cause?

A

Gouty arthritis
Tophi (aggregated deposits of MSU in tissue)
Extreme pain

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15
Q

What does gouty arthritis commonly affect?

A

Metatarsophalangeal joint of the big toe (‘1st MTP joint’)

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16
Q

What are the affects of gouty arthritis?

A

Abrupt onset
Extremely painful
Joint red, warm, swollen and tender
Resolves spontaneously over 3-10 days

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17
Q

What investigation is done in gout?

A

Joint aspiration – synovial fluid analysis

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18
Q

What is the management of gout?

A

Acute attack – colcihine, NSAIDs, Steroids

Chronic – allopurinol

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19
Q

What are synovial fluid samples examined for?

A

Pathogens
Crystals
Rapid Gram stain followed by culture and antibiotic sensitivity assays

Polarising light microscopy to detect crystals which can be seen in arthritis due to gout or pseudogut

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20
Q

What are the features of synovial fluid in gout?

A

Crystal - urate
Shape - needles
Polarizing light microscopy - negative

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21
Q

What are the features of synovial fluid in pseudogout?

A

Crystal - Calcium pyrophosphate dihydrate (‘CPPD’)

Shape - brick shaped

Polarizing light microscopy - positive

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22
Q

What are the immune mediated inflammatory joint diseases?

A

SLE
Rheumatoid arthritis
Vasculitis

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23
Q

What is the most common Immune-mediated inflammatory joint disease?

A

Rheumatoid arthritis

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24
Q

What is RA?

A

chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis
(inflammation of the synovial membrane) of synovial (diarthrodial) joints

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25
Q

What is the pathogenesis of RA?

A

Synovial membrane is abnormal in rheumatoid arthritis:

The synovium becomes a proliferated mass of tissue (pannus

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26
Q

What is the dominant cytokine in RA?

A

TNF Alpha

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27
Q

How has the role of TNF alpha been proven?

A

validated by the therapeutic success of TNFα inhibition in this condition

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28
Q

How is TNF alpha inhibited

A

TNFα inhibition is achieved through parenteral administration (most commonly sub-cutaneous injection) of antibodies or fusion proteins

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29
Q

What are the key features of RA?

A

Polyarthritis - swelling of the small joints of the hand and wrists is common
Symmetrical
Early morning stiffness in and around joints
May lead to joint damage and destruction - ‘joint erosions’ on radiographs

30
Q

What are the extra-articular manifestation of RA?

A

Rheumatoid nodules

Others rare e.g. vasculitis, episcleritis

31
Q

What might be detected in the blood in RA?

A

Rheumatoid factor

Autoantibody against IgG - should really call this rheumatoid ‘antibody’ not ‘factor’

32
Q

What is the joint pattern of involvement in RA?

A

Affects small and large joints, but particularly hands and feet
Symmetrical
Affects multiple joints (polyarthritis)

33
Q

Which joints are most affected by RA?

A 
Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
Wrists 
Knees
Ankles
Metatarsophalangeal joints (MTP)
34
Q

What are the effects of synovial inflammation?

A

joint synovitis
tenosynovitis
bursa

35
Q

What are common extra-articular features?

A

Fever, weight loss

Subcutaneous nodules

36
Q

What are less common extra-articular features?

A

vasculitis
Ocular inflammation e.g. episcleritis
Neuropathies
Amyloidosis
Lung disease – nodules, fibrosis, pleuritis
Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis

37
Q

What are subcutaneous nodules?

A

Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue
Occur in ~30% of patients

38
Q

What are subcutaneous nodules associated with?

A

Severe disease
Extra-articular manifestations
Rheumatoid factor

39
Q

What is rheumatoid factors?

A

Antibodies that recognize the Fc portion of IgG as their target antigen
typically IgM antibodies i.e. IgM anti-IgG antibody

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

40
Q

What are the second type of antibodies seen in RA?

A

Antibodies to citrullinated protein antigens

41
Q

What are ACPA’s?

A

highly specific for rheumatoid arthritis
Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’
Citrullination of peptides is mediated by enzymes termed:
Peptidyl arginine deiminases (PADs)

42
Q

What is the treatment goal in RA?

A

Prevent joint damage

43
Q

What are the requirements regarding management?

A

Early recognition of symptoms, referral and diagnosis
Prompt initiation of treatment: joint destruction = inflammation x time
Aggressive treatment to suppress inflammation

44
Q

What is the drug treatment in RA?

A

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

45
Q

What is the first line treatment for RA?

A

1st line treatment:

methotrexate in combination with hydroxychloroquine or sulfasalazine

46
Q

What is 2nd line treatment for RA?

A

2nd line:
Biological therapies offer potent and targeted treatment strategies
New therapies include Janus Kinase inhibitors : Tofacitinib & Baricitinib

47
Q

What drugs can be used short term?

A

Important roles for glucocorticoid therapy (prednisolone) but avoid long-term use because of side-effects.

48
Q

What is important in the management of RA?

A

Multidisciplinary approach also important e.g. physiotherapy, occupational therapy, hydrotherapy, surgery

49
Q

What are biologics?

A

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

50
Q

What are the main features with ankylosing spondylitis?

A

Seronegative spondyloarthropathy – no positive autoantibodies
Chronic sacroillitis – inflammation of sacroiliac joints
Results in spinal fusion – ankylosis
Common demographic: 20-30yrs, M
Associated with HLA B27

51
Q

What is the clinical presentation of AS?

A 
Lower back pain + stiffness
Early morning
Improves with exercise
Reduced spinal movements
Peripheral arthritis
Plantar Fasciitis, Achilles Tendonitis
Fatigue
52
Q

What might you find on inspection in AS?

A

Hyperextended neck
Loss of Lumbar lordosis
Flexed hips and knees

53
Q

What bloods are important in AS?

A

Normocytic anaemia
Raised CRP, ESR
HLA-B27

54
Q

What imaging is done in AS?

A

X-rays

MRI

55
Q

What would you look for on a MRI re AS?

A

Squaring Vertebral bodies, Romanus lesion
Erosion, sclerosis, narrowing SIJ
Bamboo Spine
Bone Marrow Oedema

56
Q

What is the management for AS?

A

Physiotherapy
Exercise regimes
NSAIDs
Peripheral joint disease - DMARDs

57
Q

What is psoriasis?

A

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

58
Q

What are the main features of psoriasis?

A

~10% of psoriasis patients also have joint inflammation

Unlike RA, rheumatoid factors are not present (“seronegative”)

Varied clinical presentations:

59
Q

What is classical presentation of PA?

A

Classically asymmetrical arthritis affecting IPJs

60
Q

How can PA clinically manifest?

A
  • Symmetrical involvement of small joints (rheumatoid pattern)
  • Spinal and sacroiliac joint inflammation
  • Oligoarthritis of large joints
  • Arthritis mutilans
61
Q

What investigations are done in PA?

A

X-rays of affected joints – pencil in cup abnormality
MRI – sacroiliitis and enthesitis
Bloods – no antibodies as seronegative

62
Q

What is the management for psoriatic arhritis?

A

DMARDs – methotrexate

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

63
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

64
Q

What are the extra-articular manifestations of reactive arthritis?

A

Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

65
Q

What can Reactive arthritis be a first manifestation of ?

A

HIV

Hep C

66
Q

Who is reactive arthritis often seen in?

A

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

67
Q

When does reactive arthritis occur?

A

Symptoms follow 1-4 weeks after infection and this infection may be mild

68
Q

What is the management of reactive arthritis?

A

Condition is usually self-limiting – can be managed with NSAIDS or DMARDs if required

69
Q

What is SLE?

A

a multi-system autoimmune disease

Multi-site inflammation: can affect any almost any organ.
Often joints, skin, kidneys, haematology. Also: lungs, CNS involvement

70
Q

What is SLE associated with?

A

with antibodies to self antigens (‘autoantibodies’)

Autoantibodies are directed against components of the cell nucleus (nucleic acids and proteins)

71
Q

What are the clinical tests for Lupus?

A
  1. Antinuclear antibodies (ANA):
    High sensitivity for SLE but not specific.
    A negative test rules out SLE, but a positive test does not mean SLE.
  2. Anti-double stranded DNA antibodies (anti-dsDNA Abs):
    High specificity for SLE in the context of the appropriate clinical signs
72
Q

What are the epidemiological features 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

Year 3 MSK (8 decks)

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