Rheumatoid arthritis Flashcards

(35 cards)

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
Which drugs are used in treatment of rheumatoid arthritis
Disease-modifying anti-rheumatic drugs (DMARDs) | Started early in disease
26
What is the advantage of DMARDs
Overcomes the need for long-term steroid use (glucocorticoid therapy)
27
How does DMARD therapy induce remission and prevent join damage
reducing the amount of inflammation in the synovium | slow or prevent structural joint damage e.g. bone erosions
28
Give examples of DMARDs
methotrexate sulphasalazine hydroxychloroquine Janus Kinase inhibitors (new)
29
Describe the biological therapy of rheumatoid arthritis
Inhibition of TNF-alpha B cell depletion Modulation of cell co-stimualtion Inhibition of IL-6
30
What is used in inhibition of TNF-alpha treatment of Rheumatoid arthritis
``` antibodies (infliximab, and others) fusion proteins (etanercept) ```
31
What is used in B cell depletion treatment of Rheumatoid arthritis
Rituximab | AB against B cell antigen CD20
32
What is used Modulation of cell co-stimualtion treatment of Rheumatoid arthritis
Abatacept - fusion protein
33
What is used Inhibition of IL-6 treatment of Rheumatoid arthritis
Tocilizumab (RoActemra) – antibody against IL-6 receptor Sarilumab (Kevzara) – antibody against IL-6 receptor
34
What are the disadvantages of biological therapy for Rheumatoid arthritis
Expensive | Increased infection risk
35
What is involved in controlling rheumatoid arthritis pathogenesis
Recruitment, activation and effector functions of these cells is controlled by a cytokine network