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Y2 Musculoskeletal > Rheumatoid arthritis > Flashcards

Rheumatoid arthritis Flashcards

1
Q

What is rheumatoid arthritis

A

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

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2
Q

What are the key feature of chronic arthritis

A 
Poly arthritis (swelling of small joints common)
Symmetrical
Early morning stiffness in and around joints
May lead to joint damage and destruction
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3
Q

What are some extra-articular diseases associated with rheumatoid arthritis

A

Rheumatoid nodules

Vasculitis, episcleritis (rare)

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4
Q

What may be detected in blood with rheumatoid arthritis

A

Rheumatoid factor - IgM autoantibody against IgG

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5
Q

What is the ratio of affected females to males of rheumatoid arthritis

A

3:1

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6
Q

Describe the genetic component of rheumatoid arthritis

A

-

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7
Q

Give an environmental component that contributes to rheumatoid arthritis

A

Smoking - contributes to 25% of population-attributable risk and interacts with shared epitope

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8
Q

Which joints are most commonly affected in rheumatoid arthritis

A 
Metacarpophalangeal joints (MCP)
Proximal interphalangeal joints (PIP)
Wrists 
Knees
Ankles
Metatarsophalangeal joints (MTP)
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9
Q

Where is the primary site of pathology for rheumatoid arthritis and give examples for each location

A

Synovium:
Synovial joints e.g. proximal inter-phalangeal joints
Tenosynovium e.g. extensor tenosynovitis
Bursa e.g. olecranon bursitis

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10
Q

Describe the sub-cutaneous nodules of rheumatoid arthritis

A

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

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11
Q

What are sub-cutaneous nodules of rheumatoid arthritis associated with

A

Severe disease
Extra-articular manifestations
Rheumatoid factor

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12
Q

Describe rheumatoid factor

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

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13
Q

What are antibodies to citrullinated protein antigens (ACPA)

A

Antibodies to citrullinated peptides are highly specific for rheumatoid arthritis
Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’
arginine -> citrulline by PADs

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14
Q

What is citrullination of peptides mediated by

A

Enzymes termed:

Peptidyl arginine deiminases (PADs)

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15
Q

Give examples of common extra-articular features of rheumatoid arthritis

A

Fever
Weight loss
Subcutaneous nodules

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16
Q

Give examples of uncommon extra-articular features of rheumatoid arthritis

A 
vasculitis
Ocular inflammation e.g. episcleritis
Neuropathies
Amyloidosis
Lung disease – nodules, fibrosis, pleuritis
Felty’s syndrome
17
Q

What is Felty’s syndrome

A

Triad of splenomegaly, leukopenia and rheumatoid arthritis

18
Q

What are the radiographic abnormalities seen in rheumatoid arthritis (early, later, later still)

A

Early
Juxta-articular osteopenia

Later
Joint erosions at margins of the joint

Later still
Joint deformity and destruction

19
Q

Describe the pathology of rheumatoid arthritis

A

Synovitis
Bone erosion
Pannus
Cartilage degradation

20
Q

Describe the pathogenesis of rheumatoid arthritis

A

Synovial membrane is abnormal

The synovium becomes a proliferated mass of tissue (pannus)

21
Q

What causes the synovial to become a proliferated mass of tissue in rheumatoid arthritis

A

Neovascularisation
Lymphangiogenesis
Inflammatory cells

22
Q

Which inflammatory cells are involved in the formation of a proliferated mass of tissue in rheumatoid arthritis

A

activated B and T cells
plasma cells
mast cells
activated macrophages

23
Q

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

A

Cytokine tumour necrosis factor-alpha (TNF-alpha)

pleotropic actions are detrimental in this setting

24
Q

What is the treatment goal for rheumatoid arthritis and what does it require

A

Prevent joint damage

Multidisciplinary approach (physiological, occupational, hydrotherapy, surgery)
Medication
Glucocorticoid therapy
Biological therapies

25
Q

Which drugs are used in treatment of rheumatoid arthritis

A

Disease-modifying anti-rheumatic drugs (DMARDs)

Started early in disease

26
Q

What is the advantage of DMARDs

A

Overcomes the need for long-term steroid use (glucocorticoid therapy)

27
Q

How does DMARD therapy induce remission and prevent join damage

A

reducing the amount of inflammation in the synovium

slow or prevent structural joint damage e.g. bone erosions

28
Q

Give examples of DMARDs

A

methotrexate
sulphasalazine
hydroxychloroquine
Janus Kinase inhibitors (new)

29
Q

Describe the biological therapy of rheumatoid arthritis

A

Inhibition of TNF-alpha
B cell depletion
Modulation of cell co-stimualtion
Inhibition of IL-6

30
Q

What is used in inhibition of TNF-alpha treatment of Rheumatoid arthritis

A 
antibodies (infliximab, and others)
fusion proteins (etanercept)
31
Q

What is used in B cell depletion treatment of Rheumatoid arthritis

A

Rituximab

AB against B cell antigen CD20

32
Q

What is used Modulation of cell co-stimualtion treatment of Rheumatoid arthritis

A

Abatacept - fusion protein

33
Q

What is used Inhibition of IL-6 treatment of Rheumatoid arthritis

A

Tocilizumab (RoActemra) – antibody against IL-6 receptor

Sarilumab (Kevzara) – antibody against IL-6 receptor

34
Q

What are the disadvantages of biological therapy for Rheumatoid arthritis

A

Expensive

Increased infection risk

35
Q

What is involved in controlling rheumatoid arthritis pathogenesis

A

Recruitment, activation and effector functions of these cells is controlled by a cytokine network

Y2 Musculoskeletal (9 decks)

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