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BRS YR2 > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is rheumatology?

A

medical speciality of diseases of the MSK system

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2
Q

What is a tendon?

A

cords of strong fibrous collagen tissue attaching muscle to bone

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3
Q

What is a ligament?

A

flexible fibrous tissue with connects 2 bones

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4
Q

What is synovium?

A

1-3 deep cell lining containing:

  • macrophage-like phagocytic cells (type A synoviocyte)
  • fibroblast-like cells that produce hyaluronic acid (type B synoviocyte)
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5
Q

What is synovial fluid?

A

hyaluronic acid-rich viscous fluid

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6
Q

What is articular cartilage?

A
  • Type 2 collagen

- proteoglycan (aggrecan)

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7
Q

What are the main 2 different types of arthritis?

A
  • osteoarthritis (degenerative)

- inflammatory (rheumatoid)

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8
Q

What is inflammation?

A

a physiological response to deal with injury or infection

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9
Q

How does inflammation manifest?

A
  • red
  • painful
  • hot
  • swelling
  • loss of function
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10
Q

What are the physiological, cellular and molecular changes caused by inflammation?

A
  • increased blood flow
  • WBC migration (leukocytes) into tissues
  • activation/differentiation of leucocytes
  • cytokine production
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11
Q

What are the different causes of joint inflammation?

A
  • crystal arthritis (gout/pseudogout)
  • autoimmune
  • inflection
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12
Q

What are some examples of different autoimmune causes of joint inflammation?

A
  • rheumatoid arthritis
  • seronegative spondyloarthropathies
  • connective tissue diseases
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13
Q

What is gout?

A

a syndrome caused by the deposition of uric crystals leading to inflammation

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14
Q

What are the causes of hyperuricaemia?

A
  • genetic tendency
  • increased intake of purine rich food
  • reduced excretion (kidney failure)
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15
Q

What is pseudogout?

A

a syndrome cause by the deposition of calcium pyrophosphate dehydrate (CPPD) crystal deposition.

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16
Q

What are the risk factors of developing pseudogout?

A
  • Hx osteoarthritis
  • elederly
  • intercurrent infection
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17
Q

How does gout arthritis present?

A
  • metatarophalangeal joint of the big toe (juxta-articular erosions)
  • sudden onset
  • painful
  • joint: red, warm, swollen and tendon
  • resolves spontaneously
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18
Q

What investigation is done in suspected gout arthritis?

A

joint aspiration: synovial fluid analysis

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19
Q

What management is done in suspected gout arthritis?

A

acute:
- colcihine
- NSAIDs
- Steroids
chronic:
- allopurinol

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20
Q

What is tested in a synovial fluid test?

A
  • gram stain, culture and ABx sensitivity

- light microscopy to stop what is in here brain

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21
Q

What is the shape of the gout crystal?

A

needle

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22
Q

What is the shape of the pseudogout crystal?

A

brick-shaped

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23
Q

What is rheumatoid arthritis?

A

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

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24
Q

What happens in rheumatoid arthritis?

A

synovium becomes a proliferate mass of tissue

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25
Q

What causes the synovium to become a proliferated mass of tissue?

A
  • neovascularisation
  • lymphangiogenensis
  • activated B and T cells
  • plasma cells
  • mast cells
  • activated macrophages
  • excess of pro-inflammatory cytokines
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26
Q

What is the dominant pro-inflammatory cytokine in rheumatoid arthritis?

A
  • TNF-alpha
  • produced by activated macrophages
  • inhibition prevents the release of IL1/6/8
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27
Q

What is the impact of the excess TNF-alpha production?

A
  • osteoclast activation
  • chemokine release
  • endothelial cell activation
  • leukocyte accumulation
  • angiogenesis
  • chondrocyte activation
  • pro-inflammatory cytokine release
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28
Q

What are the key features of rheumatoid arthritis?

A
  • polyarthritis (swelling of small joints)
  • symmetrical
  • early morning stiffness
  • may cause joint damage and destruction
  • rheumatoid nodules
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29
Q

What can be used to detect rheumatoid arthritis?

A

rheumatoid factor, autoantibody against IgE

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30
Q

What are the most commonly affected joints with rheumatoid arthritis?

A
  • Metacarpophalangeal joints (MCP)
  • Proximal interphalangeal joints (PIP)
  • Wrists
  • Knees
  • Ankles
  • Metatarsophalangeal joints (MTP)
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31
Q

Where is the primary site of the pathology of rheumatoid arthritis?

A
  • synovial joints
  • tenosynovium surrounding tendons
  • bursa
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32
Q

What are the extra-articular features of rheumatoid arthritis?

A
  • fever
  • weight loss
  • subcutaneous nodules
  • vasculitis
  • ocular inflammation
  • neuropathies
  • amyloidosis
  • lung disease (nodules, fibrosis and pleuritis)
  • Felty’s syndrome
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33
Q

What is Felty’s syndrome?

A
  • slpnomegaly
  • leukopenia
  • rheumatoid arthritis
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34
Q

What are subcutaneous nodules in rheumatoid arthritis?

A

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

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35
Q

What are subcutaneous nodules associated with?

A
  • severe disease
  • extra-articular manifestations
  • rheumatoid factor
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36
Q

Where do subcutaneous nodules tend to be found?

A
  • the ulnar border of the forearm

- in the hands

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37
Q

What antibodies are found in those with rheumatoid arthritis?

A
  • rheumatoid factor

- antibodies to citrullinated protein antigens

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38
Q

What is a rheumatoid factor?

A
  • Antibodies that recognize the Fc portion of IgG as their target antigen
    (typically IgM antibodies i.e. IgM anti-IgG antibody)
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39
Q

What are antibodies to citrullinated protein antigens?

A
  • Citrullination of peptides is mediated by enzymes termed:

Peptidyl arginine deiminases (PADs)

40
Q

What does rheumatoid arthritis treatment require?

A
  • Early recognition of symptoms, referral and diagnosis
  • Prompt initiation of treatment
    (joint destruction = inflammation x time)
  • Aggressive treatment to suppress inflammation
41
Q

What is the first line treatment of rheumatoid arthritis?

A

methotrexate in combination with hydroxychloroquine or sulfasalazine

42
Q

What is the second line treatment of rheumatoid arthritis?

A
  • Biological therapies offer potent and targeted treatment strategies
  • New therapies include Janus Kinase inhibitors : Tofacitinib & Baricitini
43
Q

What drugs are involved in the treatment of rheumatoid arthritis?

A

Disease-modifying, anti rheumatic drugs

44
Q

What are the targets of the biologics used in the treatment of rheumatoid arthritis?

A
  • Inhibition of tumour necrosis factor-alpha (‘anti-TNF’)
  • B cell depletion
  • Modulation of T cell co-stimulation
  • Inhibition of IL-6 signalling
45
Q

What is the mechanism of infliximab and etanercept?

A

Inhibition of tumour necrosis factor-alpha (‘anti-TNF’)

46
Q

What is the mechanism of rituximab?

A

B cell depletion

47
Q

What is the mechanism of Abatacept?

A

Modulation of T cell co-stimulation

48
Q

What is the mechanism of Tocilizumab and Sarilumab?

A

Inhibition of interleukin-6 signalling

49
Q

How does Ankylosing spondylitis present?

A
  • lower back pain (>3months) and stiffness (early morning, better with exercise)
  • reduced spinal movements
  • peripheral arthritis
  • plantar faciitis
  • achilles tendonitis
  • fatigue
50
Q

What are the visual signs of Ankylosing spondylitis?

A
  • hyperextended neck
  • loss of lumbar lordosis
  • flexed hips and knees
51
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

52
Q

What are the extra-articular features of reactive arthritis?

A
  • Enthesitis (tendon inflammation)
  • Skin inflammation
  • Eye inflammation
53
Q

What can reactive arthritis be a sign of?

A
  • HIV

- Hep C

54
Q

How do you treat reactive arthritis?

A

self-limiting

  • NSAIDs
  • DMARDs
55
Q

What are the risk factors of reactive arthritis?

A
  • genetic predisposition and environmental trigger
56
Q

How long does it take for reactive arthritis to present after an infection?

A

1-4 weeks

57
Q

What is Psoriasis?

A

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

58
Q

Can you use rheumatoid factors to diagnose psoriatic arthritis?

A

not present (seronegative)

59
Q

How does Psoriatic arthritis present?

A
  • Classically asymmetrical arthritis affecting IPJs
  • Symmetrical involvement of small joints (rheumatoid pattern)
  • Spinal and sacroiliac joint inflammation
  • Oligoarthritis of large joints
  • Arthritis mutilans
60
Q

What investigations can be done for suspected Psoriatic arthritis?

A
  • XR of affected joints

- MRI (scaroiliitis and enhteisitis)

61
Q

What is the management plan for Psoriatic arthritis?

A
  • DMARDs (methotrexate)

- avoid oral steroids

62
Q

What is lupus?

A

a multi-system autoimmune disease associated with antibodies to self antigens (‘autoantibodies’) which are directed against components of the cell nucleus

63
Q

What is associated with lupus?

A
  • Multi-site inflammation: can affect any almost any organ.
  • Often joints, skin, kidneys, haematology.
  • Also: lungs, CNS involvement
64
Q

What clinical tests can be done when lupus is suspected?

A
  • Antinuclear antibodies (ANA)

- Anti-double stranded DNA antibodies (anti-dsDNA Abs):

65
Q

Why are antinuclear antibodies measured for suspected lupus?

A
  • High sensitivity for SLE but not specific.

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

66
Q

Why are Anti-double stranded DNA antibodies measured for suspected lupus?

A

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

67
Q

When is lupus most common?

A
  • 15-40 years old

- asian and african populations

68
Q

What is management plan for Ankylosing spondylitis?

A
  • physiotherapy
  • exercise regimes
  • NSAIDs
  • peripheral joint deposition (DMARDs)
69
Q

Can you definitively test for Ankylosing spondylitis?

A

no, seronegative spondyloarthropathy – no positive autoantibodies

70
Q

What happens in Ankylosing spondylitis?

A
  • Chronic sacroillitis (inflammation of sacroiliac joints)

- Results in spinal fusion (ankylosis) and deformity

71
Q

What is Ankylosing spondylitis associated with?

A

HLA B27

72
Q

When is Ankylosing spondylitis most common?

A
  • 20-30 years old

- male

73
Q

What tests should be done in suspected Ankylosing spondylitis?

A
  • FBC
  • CRP, ESR
  • test for HLA-B27
  • XR
  • MRI
74
Q

What would blood tests show in Ankylosing spondylitis?

A

FBC: normocytic anaemia
CRP, ESR: raised
HLA-B27: present

75
Q

What would imaging (MRI/XR) show in Ankylosing spondylitis?

A
  • Squaring Vertebral bodies, Romanus lesion
  • Erosion, sclerosis, narrowing SIJ
  • Bamboo Spine
  • Bone Marrow Oedema
76
Q

What are some other examples of connective tissue disorders?

A
  • Systemic Sclerosis
  • Myositis
  • Sjogrens syndrome
  • Mixed connective tissue disease
77
Q

What is the site of inflammation in Ankylosing spondylitis?

A

enthesis

78
Q

what are the seronegative spondyloarthropathies?

A
  • Ankylosing spondylitis
  • Reactive Arthritis (Reiters syndrome)
  • Psoriatic arthritis
  • Arthritis associated with GI inflammation (enteropathic synovitis)
79
Q

What is SLE?

A

Chronic tissue inflammation in the presence of antibodies directed against self antigens
(multi-site inflammation: joints, skin and kidney)

80
Q

What autoantibodies are associated with SLE?

A
  • Antinuclear antibodies
  • Anti-double stranded DNA antibodies
  • Anti-phospholipid antibodies
81
Q

What are the connective tissue diseases?

A
  • SLE
  • Sjogren’s syndrome
  • Autoimmune Inflammatory muscle disease
  • Systemic sclerosis (scleroderma)
  • Overlap syndromes
82
Q

What is common in connective tissue disorders?

A

Reynaud’s phenomenon

83
Q

What is Reynaud’s phenomenon?

A

Intermittent vasospasm of digits on exposure to cold
(white to blue to red)
- leads to blanching of digit
- Cyanosis as static venous blood deoxygenates
- Reactive hyperaemia

84
Q

What information do serum autoantibodies provide?

A
  • correlate to disease activity
  • directly pathogenic
  • can aid in diagnosis
85
Q

What is typically non-erosive?

A
  • arthralgia

- arthritis

86
Q

When is SLE typically diagnosed?

A

in females aged 15-45 years old

87
Q

What are the different clinical manifestations of SLE?

A
  • Malar rash
  • Photosensitive rash
  • Mouth ulcers
  • Hair loss
  • Raynaud’s phenomenon
  • Arthralgia and sometimes arthritis
  • Serositis (pericarditis, pleuritis, less commonly peritonitis)
  • Renal disease – glomerulonephritis (‘lupus nephritis’)
  • Cerebral disease – ‘cerebral lupus’ e.g. psychosis
88
Q

What is a Malar rash?

A

erythema that spares the nasolabial fold

89
Q

What is the pathogenesis of SLE?

A
  • Apoptosis leads to translocation of nuclear antigens to membrane surface
  • Impaired clearance of apoptotic cells results in enhanced presentation of nuclear antigens to immune cells
  • B cell autoimmunity
  • Tissue damage by antibody effector mechanisms e.g. complement activation and Fc receptor engagement
90
Q

What are anti-phospholipid antibodies associated with?

A

risk of arterial and venous thrombosis

91
Q

What autoantibodies are associated with systemic vasculitis?

A

antinuclear cytoplasmic antibodies (ANCA)

92
Q

What is the significance of antinuclear antibodies in SLE?

A
  • seen in all SLE cases

- not specific for SLE

93
Q

What is the significance of anti-double stranded DNA antibodies in SLE?

A
  • specific to SLE

- serum level correlates to disease activity

94
Q

What is the significance of anti-phospholipid antibodies in SLE?

A
  • associated with risk of arterial and venous thrombosis in SLE
  • may also occur in absence of SLE in what is termed the ‘primary anti-phospholipid antibody syndrome
95
Q

What is the significance of anti-Sm antibodies in SLE?

A
  • specific to SLE

- serum level does not correlate to disease activity

96
Q

What is the significance of anti-Ro and Anti-La antibodies in SLE?

A
  • secondary sjögren’s syndrome

- neonatal lupus syndrome (transient rash, permanent heart block)

97
Q

What is the significance of anti-ribosomal P antibodies in SLE?

A

cerebral lupus

BRS YR2 (70 decks)

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