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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 which 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 made of?

A
  • Type 2 collagen
  • proteoglycan (aggrecan)
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7
Q

What is arthirtis?

A

Disease of the joints

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8
Q

What are the main 2 different types of arthritis?

A
  • osteoarthritis (degenerative)
  • inflammatory (rheumatoid)
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9
Q

What is inflammation?

A

a physiological response to deal with injury or infection

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10
Q

How does inflammation manifest?

A
  • red
  • painful
  • hot
  • swelling
  • loss of function
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11
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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12
Q

What are the different causes of joint inflammation?

A
  • crystal arthritis (gout/pseudogout)
  • immune-mediated
  • infection
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13
Q

What are the different infectious causes of joint inflammation?

A
  • septic arthiritis
  • tuberculosis
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14
Q

Which causes of joint inflammation are primary and secondary?

A
  • immune mediated = primary inflammation
  • infection and crystal arthiritis = secondary inflammation in response to noxious insult
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15
Q

Which causes of inflammation are sterile and non sterile?

A
  • crystal arthirtis and immune-mediated = sterile
  • infection = nonsterile
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16
Q

What should be assumed when a patient presents with an acute hot, swollen joint

A

Septic arthiritis because it is a medical emergency

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17
Q

What is the key investigation for septic arthiritis?

A

Joint aspiration, send fluid for gram stain and culture

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18
Q

What is the management for septic arthiritis?

A
  • Joint lavage
  • IV antibiotics
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19
Q

What are some examples of different immune-mediated causes of joint inflammation?

A
  • rheumatoid arthritis
  • seronegative spondyloarthropathies
  • connective tissue diseases
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20
Q

What is gout?

A

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

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21
Q

What is pseudogout?

A

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

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22
Q

What is tested in a synovial fluid test?

A
  • gram stain, culture and ABx sensitivity
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23
Q

What is rheumatoid arthritis?

A
  • chronic autoimmune disease
  • characterised by pain, stiffness and symmetrical synovitis
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24
Q

What is synovitis?

A

Inflammation of the synovial membrane

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25
Q

What happens in rheumatoid arthritis?

A

synovium becomes a proliferated mass of tissue (pannus)

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26
Q

What is the aetiology of rheumatoid arthiritis?

A

Genetic and environmental

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27
Q

What are some environmental risk factors for rheumatoid arthirits?

A
  • smoking
  • microbiome
  • P. gingivalis
  • poor oral health
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28
Q

What do both smoking and P. gingivalis cause?

A

Citrullination of proteins in the lung epithelium

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29
Q

What are the genetic risk factors for rheumatoid arthiritis?

A
  • female sex
  • HLA-DR shared epitope
  • cumulative genetic burden of other genetic loci (polygenic disease)
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30
Q

What are class 1 HLAs?

A
  • HLA A, B and C
  • expressed on all cells
  • presented with antigen to CD8 T cells
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31
Q

What are class 2 HLAs?

A
  • HLA D
  • only expressed on APCs
  • presented with antigen to CD4 T cells which stimulates B cells
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32
Q

Why are autoantibodies found in rheumatoid arthirtis but not ankylosing spondylitis?

A
  • ankylosing spondylitis is associated with class 1 HLA (HLAB27)
  • rheumatoid arthirits associated with class 2 HLA (HLADR4)
  • only class 2 HLAs stimulate B cells which secrete antibodies
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33
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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34
Q

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

A
  • TNF-alpha
  • IL-6, IL-1
  • produced by activated macrophages
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35
Q

Which cells are invloved in the pathogenesis of rheumatoid arthiritis?

A

Autoreactive B and T cells

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36
Q

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

A
  • osteoclast activation
  • chemokine release
  • endothelial cell activation
  • leukocyte accumulation
  • angiogenesis
  • lymphangiogenesis
  • inflammatory cell recruitment
  • matrix metalloproteinases
  • chondrocyte activation
  • pro-inflammatory cytokine release
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37
Q

What causes pannus formation?

A
  • inflammatory cell recruitment
  • angiogenesis
  • lymphangiogenesis
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38
Q

What do matrix metalloproteinases cause?

A

Cartilage loss

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39
Q

What does osteoclast activation cause?

A

bone loss

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40
Q

What are the key features of rheumatoid arthritis?

A
  • chronic
  • polyarthritis (swelling of small joints)
  • symmetrical
  • early morning stiffness
  • may cause joint damage and destruction
  • rheumatoid nodules
  • systemic with extra-articular manifestations
  • autoantibodies usually detected in blood
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41
Q

What can be used to detect rheumatoid arthritis?

A

rheumatoid factor, autoantibody against IgE

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42
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)
  • nearly always invloves small joints
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43
Q

Where are the primary sites of the pathology of rheumatoid arthritis?

A
  • synovial joints
  • tenosynovium surrounding tendons
  • bursa
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44
Q

What are the extra-articular features of rheumatoid arthritis?

A
  • fever
  • fatigue
  • weight loss
  • subcutaneous nodules
  • vasculitis
  • ocular inflammation
  • neuropathies
  • amyloidosis
  • lung disease (nodules, fibrosis and pleuritis)
  • Felty’s syndrome
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45
Q

What is Felty’s syndrome?

A
  • splenomegaly
  • leukopenia
  • rheumatoid arthritis
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46
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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47
Q

What are subcutaneous nodules associated with?

A
  • severe disease
  • extra-articular manifestations
  • rheumatoid factor
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48
Q

Where do subcutaneous nodules tend to be found?

A
  • the ulnar border of the forearm
  • in the hands
49
Q

Which blood tests are done for rheumatoid arthiritis?

A
  • ESR
  • CRP
  • PLT
  • autoantibodies
  • all increased
50
Q

What antibodies are found in those with rheumatoid arthritis?

A
  • rheumatoid factor
  • antibodies to citrullinated protein antigens (anti-CCP)
51
Q

Is rheumatoid factor only present in people with rheumatoid arthiritis?

A

No

52
Q

What imaging is done for rheumatoid arthiritis?

A
  • X-ray
  • US (best at picking it up early)
  • MRI
53
Q

What are the features of rheumatoid arthiritis which show on a radiograph?

A
  • soft tissue swelling
  • peri-articular osteopenia
  • bony erosions
  • limited to information on bony structures only
54
Q

Which ultrasound changes are seen in rheumatoid arthirtis?

A
  • synovial thickening
  • increased blood flow
  • erosions which can’t be seen on plain radiograph
55
Q

Which imaging is used in sn early arthiritis clinic?

A

Ultrasound

56
Q

What does rheumatoid arthritis treatment require?

A
  • Early recognition of symptoms, referral and diagnosis
  • Prompt initiation of treatment
  • Aggressive treatment to suppress inflammation
  • multidisciplinary input
  • goal is to prevent joint damage
57
Q

What are the main pharmological treatments for rheumatoid arthiritis?

A
  • glucocorticoid therapy (acute use)
  • disease-modifying anti-rheumatic drugs (DMARDS)
58
Q

What is the action of glucocorticoids?

A
  • bind to GR receptor in cytoplasm
  • steroid-GR complex translocates to nucleus and binds to DNA
  • affects transcription
59
Q

What are the different methods of steroid administration?

A
  • oral
  • intramuscular
  • intravenous
  • intra-articular
60
Q

What are the side effects of steroid use?

A

Cushing’s syndrome

61
Q

What is the first line treatment of rheumatoid arthritis?

A
  • DMARD therapy (methotrexate in combination with hydroxychloroquine or sulfasalazine)
  • IM or oral steroids
62
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
63
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
64
Q

What is treat to target?

A
  • suppress disease activity to improve outcome
  • uses DAS28
65
Q

What is DAS28?

A
  • score, if not suppressed then escalate treatment
  • number of tender joints
  • number of swollen joints
  • patient visual analogue score
  • ESR/CRP
66
Q

What is the mechanism of infliximab and etanercept?

A
  • Inhibition of tumour necrosis factor-alpha (‘anti-TNF’)
  • infliximab targets antibodies
  • entanercept targets fusion proteins
67
Q

What is the mechanism of rituximab?

A
  • B cell depletion
  • antibody against B cell antigen CD20
68
Q

What is the mechanism of Abatacept?

A
  • Modulation of T cell co-stimulation
  • blocks CD80/CD86 on APC binding to CD28 on T cell
69
Q

What is the mechanism of Tocilizumab and Sarilumab?

A

Inhibition of interleukin-6 signalling

70
Q

What is seronegative arthiritis?

A
  • inflammatory arthiritis where RF and CCP antibodies are not present in blood
  • still immune mediated
71
Q

What are the different types of seronegative arthiritis?

A
  • psoratic arthiritis
  • reactive arthiritis
  • ankylosing spondylitis
  • IBD-associated arthiritis
72
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
73
Q

What are the extra-articular features of reactive arthritis?

A
  • Enthesitis (tendon inflammation)
  • Skin inflammation
  • Eye inflammation
74
Q

What can reactive arthritis be a sign of?

A
  • HIV
  • Hep C
75
Q

What are the risk factors of reactive arthritis?

A
  • genetic predisposition (HLA-B27) and environmental trigger
76
Q

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

A

1-4 weeks

77
Q

What is Psoriasis?

A
  • an autoimmune disease affecting the skin
  • scaly red plaques on extensor surfaces eg elbows and knees
  • 10% of patients have joint inflammation
78
Q

What is the dominant pathogenic pathway for psoratic arthiritis?

A

IL-17 and IL-23

79
Q

What is the relationship between skin disease and joint manifestations of psoratic arthiritis?

A
  • skin disease severity is not correlated to joint manifestations
  • nail changes may be the only skin manifestations
  • need to carefully examine the skin for small areas of psoriasis
80
Q

How does Psoriatic arthritis present?

A
  • Classically asymmetrical arthritis affecting IPJs
  • Enthisitis
  • Symmetrical involvement of small joints (rheumatoid pattern)
  • Spinal and sacroiliac joint inflammation
  • Oligoarthritis of large joints
  • Arthritis mutilans
81
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

82
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
83
Q

What clinical tests can be done when lupus is suspected?

A
  • Antinuclear antibodies (ANA)

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

84
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.

85
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.

86
Q

When is lupus most common?

A
  • 15-40 years old

- asian and african populations

87
Q

What is management plan for Ankylosing spondylitis?

A
  • physiotherapy
  • exercise regimes
  • NSAIDs
  • peripheral joint deposition (DMARDs)
88
Q

Can you definitively test for Ankylosing spondylitis?

A

no, seronegative spondyloarthropathy – no positive autoantibodies

89
Q

What happens in Ankylosing spondylitis?

A
  • Chronic sacroillitis (inflammation of sacroiliac joints)

- Results in spinal fusion (ankylosis) and deformity

90
Q

What is Ankylosing spondylitis associated with?

A

HLA B27

91
Q

When is Ankylosing spondylitis most common?

A
  • 20-30 years old

- male

92
Q

What tests should be done in suspected Ankylosing spondylitis?

A
  • FBC
  • CRP, ESR
  • test for HLA-B27
  • XR
  • MRI
93
Q

What would blood tests show in Ankylosing spondylitis?

A

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

94
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
95
Q

What are some other examples of connective tissue disorders?

A
  • Systemic Sclerosis
  • Myositis
  • Sjogrens syndrome
  • Mixed connective tissue disease
96
Q

What is the site of inflammation in Ankylosing spondylitis?

A

enthesis

97
Q

what are the seronegative spondyloarthropathies?

A
  • Ankylosing spondylitis
  • Reactive Arthritis (Reiters syndrome)
  • Psoriatic arthritis
  • Arthritis associated with GI inflammation (enteropathic synovitis)
98
Q

What is SLE?

A

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

99
Q

What autoantibodies are associated with SLE?

A
  • Antinuclear antibodies
  • Anti-double stranded DNA antibodies
  • Anti-phospholipid antibodies
100
Q

What are the connective tissue diseases?

A
  • SLE
  • Sjogren’s syndrome
  • Autoimmune Inflammatory muscle disease
  • Systemic sclerosis (scleroderma)
  • Overlap syndromes
101
Q

What is common in connective tissue disorders?

A

Reynaud’s phenomenon

102
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

103
Q

What information do serum autoantibodies provide?

A
  • correlate to disease activity
  • directly pathogenic
  • can aid in diagnosis
104
Q

What is typically non-erosive?

A
  • arthralgia

- arthritis

105
Q

When is SLE typically diagnosed?

A

in females aged 15-45 years old

106
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
107
Q

What is a Malar rash?

A

erythema that spares the nasolabial fold

108
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
109
Q

What are anti-phospholipid antibodies associated with?

A

risk of arterial and venous thrombosis

110
Q

What autoantibodies are associated with systemic vasculitis?

A

antinuclear cytoplasmic antibodies (ANCA)

111
Q

What is the significance of antinuclear antibodies in SLE?

A
  • seen in all SLE cases

- not specific for SLE

112
Q

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

A
  • specific to SLE

- serum level correlates to disease activity

113
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
114
Q

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

A
  • specific to SLE

- serum level does not correlate to disease activity

115
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)

116
Q

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

A

cerebral lupus

117
Q

What are the two different types of twin studies?

A
  • monozygotic twins = identical DNA
  • dizygotic twins = share 50% DNA
118
Q

What does the concordance rate of twin studies indicate?

A
  • concordance rate of monozygotic twins higher than dizygotic twins indicates genetic cause
  • if a disease is purely genetic the concordance rate for monozygotic twins is 100% the disease is purely genetic

BRS YR2 (67 decks)

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