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brs musculoskeletal > 1b// Rheumatoid and Other Inflammatory Arthritis > Flashcards

1b// Rheumatoid and Other Inflammatory Arthritis Flashcards

1
Q

What is arthritis?

A

disease of the joints

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2
Q

What are the 2 major divisions of arthritis?

A

osteoarthritis

arthritis with signs of inflammation

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3
Q

What is osteoarthritis?

A

degenerative arthritis

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4
Q

What are the clinical examination signs of joint inflammation?

A

red
hot/ warm
swelling/ fluid

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5
Q

What is this showing? (smth about space)

A

Lack of space indicates loss of articular cartilage leading to bone in contact with bone

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6
Q

What are the causes of joint inflammation?

A
  1. infection
  2. crystal arthritis
  3. immune mediated (autoimmune)
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7
Q

What are examples of joint inflammation caused by infection?

A

septic arthritis
Tuberculosis

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8
Q

What are examples of joint inflammation caused by crystal arthritis?

A

Gout
Pseudogout

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9
Q

What type of joint inflammation is secondary and primary?

A

secondary inflammation in response to a noxious insult

immune= primary inflammation

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10
Q

What type of joint inflammation is sterile and which are non-sterile?

A

infection= non-sterile

immune and crystal= sterile

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11
Q

What are the 4 major arthritis you need to know?

A

degenerative (osteoarthritis)
immune mediated
crystal arthritis
septic arthritis

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12
Q

How is the inflammation in…

degenerative (osteoarthritis)
immune mediated
crystal arthritis
septic arthritis

A

degenerative (osteoarthritis)= none or little

immune mediated= yes- autoimmune

crystal arthritis= yes- secondary to crystals

septic arthritis= yes- secondary to infections

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13
Q

How is the speed of onset with…

degenerative (osteoarthritis)
immune mediated
crystal arthritis
septic arthritis

A

degenerative (osteoarthritis)= slow

immune mediated= subacute

crystal arthritis= rapid

septic arthritis= rapid

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14
Q

What is the synovial fluid analysis like in…

degenerative (osteoarthritis)
immune mediated
crystal arthritis
septic arthritis

A

degenerative (osteoarthritis)= no inflammatory cells,sterile

immune mediated= inflammatory cells, sterile

crystal arthritis= inflammatory cells, sterile, crystals

septic arthritis= inflammatory cells and bacteria

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15
Q

What is the CRP like with…

degenerative (osteoarthritis)
immune mediated
crystal arthritis
septic arthritis

A

degenerative (osteoarthritis)= normal

immune mediated= high

crystal arthritis= high/ very high

septic arthritis= very high

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16
Q

What is the white cell count like with…

degenerative (osteoarthritis)
immune mediated
crystal arthritis
septic arthritis

A

degenerative (osteoarthritis)= normal

immune mediated= usually normal

crystal arthritis= usually normal

septic arthritis= high

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17
Q

Is septic arthritis an emergency?

A

yes an orthopaedic emergency

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18
Q

When should you assume it’s septic arthritis until proven otherwise?

A

acute, hot, swollen joint

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19
Q

What is the key investigation for septic arthritis?

A

joint aspiration
send fluid for Gram stain and culture

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20
Q

What is the management of septic arthritis?

A

joint washout (lavage) and IV antibiotics

lavage bc anti-b amy not reach

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21
Q

What are the types of autoimmune inflammatory arthritis?

A

Rheumatoid arthritis

Seronegative arthritis

Lupus and related disorders

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22
Q

How would you simply describe the clinical features rheumatoid arthritis?

A

Subacute/chronic Polyarthritis
Small & large joints
Symmetrical

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23
Q

What are the types of seronegative arthritis?

A

Psoriatic arthritis Reactive arthritis
Ankylosing spondylitis
IBD-associated

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24
Q

How would you simply describe the clinical features seronegative arthritis?

A

Subacute/chronic
Mono and/ or oligo large joint*
May involve spine
Asymmetrical

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25
Q

How would you simply describe the clinical features of lupus and related disorders?

A

Subacute/Chronic
Polyarthralgia (often little swelling)
Frank arthritis usually non-erosive

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26
Q

Describe the classification of arthritis.

A
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27
Q

What is rheumatoid arthritis?

A

Rheumatoid arthritis (RA) : synovial inflammation

chronic autoimmune disease

Systemic disease with extra-articular manifestations

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28
Q

What is the primary site of pathology of rheumatoid arthritis?

A

the synovium

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29
Q

What is the inflammation of

A
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30
Q

the synovial membrane called?

A

synovitis

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31
Q

Where is the synovium found?

A

joints= synovial diarthrodial joints

tendons= tenosynovium surrounding tendons

bursa

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32
Q

What is the sex bias and age of onset for rheumatoid arthritis?

A

F:M = 2:1

30s-50s

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33
Q

What are the key features of rheumatoid arthritis?

A

Chronic arthritis

Polyarthritis

Pain, swelling and early morning stiffness in and around joints

May lead to joint damage and destruction - ‘joint erosions’ on radiographs

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34
Q

What is normally detected in the blood with rheumatoid arthritis? And give examples.

A

Auto-antibodies usually detected in blood

such as rheumatoid factor and anti-citrullinated protein antibodies (ACPA)

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35
Q

How do you estimate the contributions of genetic vs environment for diseases?

A
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36
Q

What is the environmental aetiology of rheumatoid arthritis?

A

Smoking
Microbiome
Porphyromonas gingivalis
Poor oral health

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37
Q

Why does smoking cause rheumatoid arthritis, and give an example of something else that does this?

A

Smoking -> citrullination of proteins in lung epithelium P. gingivalis can also cause citrullination

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38
Q

Is rheumatoid arthritis genetic?

A

mixture of genes and environment

seen from twin studies
RA concordance in twins 1 : monozygotic ~15% dizygotic ~4%

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39
Q

What is the strongest genetic risk factor for rheumatoid arthritis?

A

HLA-DR

especially HLA-DR(beta)1

and HLA-DR4 (not as much)

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40
Q

What 2 synergistically increase risk of RA?

A

HLA-DRb chain amino acids 70-74 (‘shared epitope’).

Smoking & shared epitope synergistically increase risk

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41
Q

How many genetic loci found by the genome wide association studies contribute to RA risk? And give examples.

A

100 other genetic loci (polygenic)

E.g. PTPN22, IL6R

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42
Q

How would you describe the effect of a risk allele for having RA?

A

modest effect

Cumulative genetic burden rather than any one variant determines risk

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43
Q

What are the classes of HLA?

A

HLA class 1= HLA A, B, C

HLA D= class 2

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44
Q

Where are HLA class 1 expressed?

A

on all ells

45
Q

How do HLA class 1 work?

A

Cells present peptide in association with HLA class 1 to CD8 (killer) T cells

46
Q

Where are HLA class 2 expressed?

A

only expressed on professional antigen presenting cells (APCs), including dendritic cells, macrophages, B cells

47
Q

How do HLA class 2 work?

A

APCs present peptide in association with HLA class 2 to CD4 (helper) T cells

CD4 T cells provide help to B cells

48
Q

What arthritis is HLA class 1 associated with? And how does it work?

A

HLA class 1 association (eg HLA-B27 in Ankylosing spondylitis) implicates CD8 T cells in pathogenesis

49
Q

What arthritis is HLA class 2 associated with? And how does it work?

A

HLA class 2 association (HLA-DR4 in RA) implicates CD4 T cells and B cells

This fits with autoantibodies (made by B cells) in RA but not in Ank Spond

50
Q

Describe the pattern of joint involvement in rheumatoid arthritis?

A

Symmetrical

Affects multiple joints (polyarthritis)

Can affects both small and large joints, but nearly always small joints involved particularly hands and feet

51
Q

What are the commonest joints affected in rheumatoid arthritis? (6)

A
  • Metacarpophalangeal joints (MCP)
  • Proximal interphalangeal joints (PIP)
  • Wrists
  • Knees
  • Ankles
  • Metatarsophalangeal joints (MTP)
52
Q

Describe the differences between rheumatoid arthritis and osteoarthritis?

A

RA: prolonged morning and inactivity stiffness
- PIPJs, MCPJs, wrists

OA: pain worse with activity
- DIPJs, PIPJs, thumb CMC, MCPJs spared

53
Q

What are the domains of extra-articular features of rheumatoid arthritis?

A

systemic inflammation

organ-specific

54
Q

What are the systemic inflammation extra-articular features of RA?

A

fatigue (v common)
fever
weight loss

55
Q

What are the organ-specific extra-articular features of RA?

A
  • Subcutaneous nodules
  • Lung disease – nodules, interstitial lung disease (ILD)/ fibrosis, pleuritis
  • Ocular inflammation e.g. episcleritis
  • Vasculitis
  • Neuropathies
  • Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis
  • Amyloidosis
56
Q

What happens at subcutaneous nodules in RA?

A

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

57
Q

Do all patients with RA experience subcutaneous nodules?

A

no, occurs in roughly 30% of patients

58
Q

What are subcutaneous nodules in RA associated with?

A

Severe disease

Extra-articular manifestations

Rheumatoid factor

59
Q

What are the histopathological changes in RA?

A
60
Q

What are the cellular and molecular players in RA?

A
  1. Autoreactive B cells
    (treatment: rituximab)
  2. Autoreactive T cells
    (treatment: abatacept)
  3. Cytokines TNF-alpha
    Interleukin-6 (Interleukin-1)
    (treatment: anti-TNFa, anti-IL6R)
61
Q

What is in excess (cellular and molecular players) in RA?

A

Excess of pro-inflammatory vs. anti-inflammatory cytokines (‘cytokine imbalance’)

62
Q

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

A

The cytokine tumour necrosis factor-alpha (TNFα) is the dominant pro-inflammatory cytokine in the rheumatoid
synovium

63
Q

What are the actions of TNFa in rheumatoid synovium?

A

Its pleotropic actions are detrimental in this setting:
- Inflammatory cell recruitment, angiogenesis, lymphangiogenesis -> Pannus formation

  • Matrix metalloproteases -> Cartilage loss
  • Osteoclast activation -> Bone loss (erosions, osteopenia)
64
Q

What is seen in bloods for RA investigations?

A

inflamm response:
- increased ESR and CRP
- sometimes normocytic anaemia, increased PLT

65
Q

What are the autoantibodies seen in RA?

A

Rheumatoid factor (RF) = antibodies that bind IgG

Anti-CCP antibodies

66
Q

What is the most specific autoantibody for RA?

A

CCP antibodies most specific for rheumatoid arthritis and associated with more aggressive/erosive disease

67
Q

When can rheumatoid factor be positive?

A

RF can be positive in other autoimmune and infective conditions, and in individuals without disease. Therefore, RF positive in the absence of clinical features does not necessarily indicate rheumatoid arthritis

68
Q

What predates first clinical symptoms of RA?

A

ACPAs

69
Q

What do you seen in X-rays for RA?

A
70
Q

What do you see in ultrasounds for RA?

A

2) Ultrasound (US) is a much better test for detecting synovitis. US changes in RA: - Synovial thickening (synovial hypertrophy)
- Increased blood flow (seen as doppler signal)
- May detect erosions not seen on plain X-ray

US (usually of hands and wrists) can be performed alongside clinical assessment in a dedicated early arthritis clinic

71
Q

What are the negatives of MRI for RA investigations?

A

MRI can also be used but expensive and time-consuming

it’s better for harder joints to get an US

72
Q

What is the treatment goal for RA?

A

prevent joint damage

73
Q

What does prevention of joint damage in RA require?

A

Early recognition of symptoms, referral and diagnosis

Prompt initiation of treatment: joint destruction = inflammation x time

Aggressive pharmacological treatment to suppress inflammation

Multidisciplinary input where needed e.g. physiotherapy, occupational therapy, surgery

74
Q

What are the pharmacological treatments for RA?

A

glucocorticoids

DMARDs

75
Q

What should you be careful about with glucocorticoids?

A

*Glucocorticoid therapy (‘steroids’) useful acutely but avoid long-term use because of side-effects

76
Q

What are DMARDs?

A

disease modifying anti-rheumatic. drugs

immunomodulatory drugs that halt or slow the disease process

77
Q

What is the first and second line treatment for RA?

A
78
Q

Do you use NSAIDs for RA?

A

NSAIDs (non-steroidal anti-inflammatory drugs):

e.g. ibuprofen, naproxen, diclofenac

Historically used but increasingly less relevant

Can provide partial symptom relief but do not prevent disease progression

Unfavourable long-term side-effect profile

79
Q

How do glucocorticoids work?

A

Glucocorticoids bind the glucocorticoid receptor (GR)

GR resides in cytoplasm

On binding by glucocorticoids, steroid-GR complex translocates
to the nucleus and binds DNA response elements, affecting transcription

80
Q

What are methods of steroid (glucocorticoid) administration?

A

Oral prednisolone

Intramuscular (IM)

methyl prednisolone
Intravenous (IV)

Intra-articular (IA)

81
Q

What are the side effects of steroids?

A

many and bad!
Cushing’s syndrome

82
Q

What is the concept of treat to target? And how is it achieved (RA specific)?

A

suppress disease activity to improve outcome

achieved by regular objective measurement of disease activity e.g., DAS28 score

83
Q

What is involved in the DAS28 score?

A

composite of…
no. of tender joints,
no. of swollen joints,
patient visual analogue score (VAS), ESR (or CRP

84
Q

What happens if DAS28 is not suppressed?

A

escalate treatment

85
Q

What are biological therapies?

A

Biological therapies are proteins (usually antibodies) that specifically target a protein

86
Q

What are some biologics targeting cytokines? (RA specific)

A
  1. Inhibition of tumour necrosis factor-alpha (‘anti-TNF’)
  2. Inhibition of interleukin-6 (IL-6) signalling
87
Q

What are examples of Inhibition of interleukin-6 (IL-6) signalling biological therapies?

A

Antibodies against IL-6 receptor:
Tocilizumab (RoActemra) Sarilumab (Kevzara)

88
Q

What are examples of Inhibition of tumour necrosis factor-alpha (‘anti-TNF’) biological therapies?

A

antibodies (infliximab, adalimumab, golimumab, certolizumab) fusion proteins (etanercept)

89
Q

What are some biologicals that target lymphocytes? (RA specific)

A
  1. B cell depletion
    - rituximab
  2. Blocking T cell co-stimulation
    - abatacept
90
Q

How does rituximab work and how is it given?

A

Rituximab – antibody against the B cell antigen, CD20
Given as two iv infusions, 2 weeks apart
Results in rapid depletion of peripheral B cells
Usually repopulate after ~6-9 months

91
Q

What are the side effects of rituximab?

A

infusion reactions, infection, hypogammaglobulinaemia

92
Q

How does abatacept work?

A

Abatacept - fusion protein - extracellular domain of CTLA-4 linked to modified Fc portion of human
immunoglobulin G1

93
Q

What do T cells need to activate? And which one does Abatacept block?

A

T cells require 2 signals to activate:
i) MHC + peptide on APC binding to TCR on T cell
ii) CD80/CD86 on APC binding to CD28 on T cell

Abatacept blocks signal 2

94
Q

Why is seronegative inflammatory arthritis called seronegative?

A

Unlike rheumatoid arthritis, RF and CCP antibodies not present in blood (“seronegative”)
BUT they are immune-mediated

95
Q

What are seronegative inflammatory arthritis?

A

Family of conditions with overlapping clinical features and pathogenesis

96
Q

What is psoriasis?

A

Psoriasis is an immune mediated disease affecting the skin

scaly red plaques on extensor surfaces (eg elbows and knees)

roughly 10% of patients also have joint inflammation

rheumatoid factor not present so seronegative

97
Q

What is the dominant pathogenic pathway in psoriatic arthritis?

A

Dominant pathogenic pathway is interleukin-17/interleukin-23 (IL17-IL23)

98
Q

Does severity of the psoriasis affect the severity of the arthritis?

A

Skin disease severity not correlated to joint manifestations

  • Examine skin carefully for small areas of psoriasis (NB scalp, umbilicus)
  • Sometimes nail changes may be only manifestation
99
Q

What are other symptoms of psoriatic arthritis?

A

nail pitting
onycholysis

dactylitis (sausage fingers) due to enthesis

100
Q

How would you describe the clinical presentation of psoriatic arthritis?

A

Varied clinical presentations:

  • Classically asymmetrical arthritis affecting IPJs
  • Enthesitis (inflammation of tendon insertions)

But also can manifest as:
- Spinal and sacroiliac joint inflammation
-Oligoarthritis of large joints
- Arthritis mutilans
- Symmetrical involvement of small joints (rheumatoid pattern)

101
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection elsewhere in the body

  • Reactive arthritis NOT the same as infection in joints (septic arthritis)
102
Q

What are the common infections leading to ractive arthritis?

A

urogenital (e.g. Chlamydia trachomatis)

gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections)

103
Q

What are important extra-articular manifestations for reactive arthritis?

A

Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

104
Q

What may reactive arthritis be the first manifestation of?

A

Reactive arthritis may be first manifestation of HIV or hepatitis C infection

105
Q

In who is reactive arthritis common?

A

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

106
Q

When do symptoms of reactive arthritis start?

A

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

107
Q

What are the differences between reactive and septic arthritis?

A

*antibiotics not indicated for joints, but may be warranted to treat underlying infection in the case of STI

108
Q

The overall classification of arthritis.

A

brs musculoskeletal (12 decks)

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