Rheumatoid and Other Inflammatory Arthritis Flashcards

1
Q

Arthritis divisions

A

Osteoarthritis (degenerative)
Inflammatory arthritis (red, warm, swelling)

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2
Q

Secondary inflammation in response to noxious insult?

A
  1. Infection - septic arthritis and TB
  2. Crystal arthritis - gout and pseudo gout
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3
Q

Primary inflammation?

A

Autoimmune

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4
Q

Non-sterile inflammation?

A

Infection - septic arthritis and TB

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5
Q

Sterile inflammation?

A

Crystal arthritis - gout and pseudo gout
Autoimmune

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6
Q

Inflammation, onset, synovial fluid analysis, CRP and WCC in osteoarthritis?

A

Inflammation - no
Onset - slow
Synovial fluid analysis - no inflammatory cells, sterile
CRP - normal
WCC - normal

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7
Q

Inflammation, onset, synovial fluid analysis, CRP and WCC in immune-mediated arthritis?

A

Inflammation - yes - autoimmune
Onset - subacute
Synovial fluid analysis - inflammatory cells, sterile
CRP - high
WCC - normal

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8
Q

Inflammation, onset, synovial fluid analysis, CRP and WCC in crystal arthritis?

A

Inflammation - yes, secondary to crystals
Onset - rapid
Synovial fluid analysis - inflammatory cells, sterile, crystals
CRP - high or very high
WCC - normal

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9
Q

Inflammation, onset, synovial fluid analysis, CRP and WCC in septic arthritis?

A

Inflammation - yes, secondary to infection
Onset - rapid
Synovial fluid analysis - inflammatory cells, bacteria
CRP - very high
WCC - high

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10
Q

Septic arthritis presentation, investigations and management?

A

Presentation - acute hot, swollen joint
Investigations - joint aspiration, send fluid for gram stain and culture
Management - joint lavage and IV Abx

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11
Q

Rheumatoid arthritis definition and primary site?

A

Chronic autoimmune disease
Primarily at synovium

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12
Q

Synovitis?

A

Inflammation of synovial membrane
Can be at synovial joint (PIP), (extensor) tenosynovium, bursa

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13
Q

Rheumatoid arthritis key features?

A

Chronic polyarthritis
Pain, swelling and early morning stiffness
May lead to joint erosions

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14
Q

Rheumatoid arthritis risk factors?

A

(Genetics)
Smoking
Micro biome
Porphyromonas gingivalis
Poor oral health
citrulination

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15
Q

RA and anti-citrullinted protein antibodies?

A

Smoking -> citrulination of lung epithelium
P. gingivalis also causes citrulination

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16
Q

Rheumatoid strongest genetic risk factor?

A

HLA-DR
polygenic

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17
Q

HLA class 1?

A

HLA A, B, C
Expressed on all cells
Present peptide to CD8 T cells

HLA-B27 in ank spond implicates CD8 T cells

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18
Q

HLA class 2?

A

HLA D
Only on professional APCs (dendritic, macrophages, B cells)
Present peptide to CD4 T cells (which provide help to B cells)

HLA-DR4 in RA implicates CD4 T and B cells

FITS WITH AUTOANTIBODIES IN RA BUT NOT ANK

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19
Q

RA pattern of joint involvement?

A

Symmetrical, poly arthritis
MCP, PIP, wrists, knees, MTP

High small and large joints but nearly always involves small - particularly hands and feet

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20
Q

RA vs osteoarthritis hands?

A

RA - PIP, MCP, wrists. Prolonged morning and inactivity stiffness

OA - PIP, DIP, thumb CMC, pain worse with activity. MCP SPARED

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21
Q

RA extra-articular features? Systemic

A

Fatigue
Fever
Weight loss

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22
Q

RA extra-articular features? Organ specific.

A

Subcutaneous nodules
Lung disease (nodules, ILD, fibrosis, pleuritis)
Ocular inflammation (episcleritis)
Vasculitis (can lead to digital ischaemia)
Neuropathies
Felty’s syndrome
Amyloidosis

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23
Q

Felty’s syndrome?

A

Extra-articular feature of RA
Triad of splenomegaly, leukopenia and RA

24
Q

RA - subcutaneous nodules

A

Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue
Associated with severe disease, extra-articular manifestations, rheumatoid factor

Typical position - forearm, PIPs

25
Healthy synovial membrane?
1-3 cell layer that lines synovial joints Contains - macrophage-like cells (type A synoviocyte), fibroblast-like cells (type B synoviocyte), type I collagen *maintains synovial fluid*
26
Synovial membrane in RA?
Synovium becomes a proliferated mass of tissue (pannus) due to: Neovascularisation Lymphangiogenesis Inflammatory cells
27
Which inflammatory cells cause synovium to become proliferated mass of tissue?
Activated B and T cells Plasma cells Mast cells Activated macrophages
28
Pannus?
Proliferated mass of tissue
29
RA pathogenesis with treatments? B, T and cytokines
1. Auto reactive B cells. Treatment - rituximab 2. Auto reactive T cells. Treatment - abatacept 3. Cytokines - TNF-a, IL-6, (IL-1). Treatment - anti-TNF-a, anti IL-6R
30
TNF-alpha in RA?
Dominant pro-inflammatory cytokine in rheumatoid synovium
31
TNF-a actions in RA?
Inflammatory cell recruitment, angiogenesis, lymphangiogenesis -> pannus formation Matrix metalloproteases -> cartilage loss Osteoclast activation -> bone loss
32
RA bloods?
Increased ESR, CRP Sometimes normocytic anaemia, increased PLT *Rheumatoid factor, anti-CCP antibodies*
33
RA autoantibodies?
Rheumatoid factor - binds IgG, can be positive in other conditions Anti-CCP antibodies - most specific, suggest more aggressive/erosive disease
34
RA steps to symptoms?
Genetic predisposition -> pre-clinical autoimmunity -> tissue inflammation and disease (symptomatic) *RF and ACPAs precede symptom onset*
35
Radiographic features of RA? X-rays
Soft tissue swelling Peri-articular osteopenia Bone erosions
36
RA ultrasound signs?
Synovial thickening (synovial hypertrophy) Increased blood flow (Doppler signal) Erosions *much better at detecting synovitis*
37
DMARDs?
Disease-modifying anti-rheumatic drugs Immunomodulatory drugs that halt or slow the disease process
38
RA first line pharmacological treatment?
Combination of DMARD therapy: Methotrexate + hydroxychloroquine and/or sulfasalazine PLUS Steroids
39
RA second line pharmacological treatment?
Biological therapies (usually therapeutic monoclonal antibodies) e.g. TNF-alpha blockade
40
Glucocorticoids MOA?
Bind glucocorticoid receptor (in cytoplasm) Steroid-GR complex translocates to nucleus and binds DNA response elements, affecting transcription
41
DAS28 score?
Used to calculate disease Includes number of tender joints, number of swollen joints, visual analogue score, and ESR (or CRP)
42
Biological therapies targeting cytokines?
1. Anti-TNF - Infliximab, adalimumab 2. Anti-IL6 (tocilizumab)
43
Biological therapies targeting lymphocytes?
1. B cell depletion - rituximab - antibody against B cell antigen CD20 2. Blocking T cell co-stimulation - blocks CD80/CD86 on APC binding to CD28 on T cell
44
Seronegative arthritis examples?
Psoriatic arthritis Ankylosing spondylitis Reactive arthritis
45
Seronegative arthritis autoantibodies?
None present. NO anti-CCP nor RF.
46
Psoriatic arthritis?
Psoriasis - immune-mediated disease affecting the skin. Scaly red plaques on extensor surfaces. 10% also have joint inflammation Seronegative.
47
Psoriatic arthritis pathogenic pathway? IL
IL-17/IL-23
48
Psoriatic arthritis signs?
Nail pitting, onycholitis, dactylitis Asymmetrical affecting IPJs Enthesitis *can also manifest as spinal and sacroiliac joint inflammation, oligoarthritis of large joints, arthritis mútilas, symmetrical small joints*
49
Reactive arthritis?
Sterile inflammation in joints following infections elsewhere in body (usually after 1-4 weeks)
50
Reactive arthritis common infections?
Urogenital (chlamydia trachomatis) Gastrointestinal (salmonella, shigella, campylobacter)
51
Reactive arthritis extra-articular manifestations?
Enthesitis Skin inflammation Eye inflammation
52
Septic arthritis vs reactive arthritis synovial fluid culture?
Septic - positive Reactive - negative
53
Septic arthritis vs reactive arthritis antibiotic therapy?
Septic - yes, IV Reactive - no, unless to treat underlying cause
54
Septic arthritis vs reactive arthritis joint lavage?
Septic - yes Reactive - no
55
Osteoarthritis LOSS?
Loss of joint space Osteophytes Sclerosis Subchondral cysts
56
Heberden’s vs Bouchard’s?
Heberden’s - DIPs Bouchard’s - PIPs *osteoarthritis*
57
Swan neck sign?
Chronic deformity of fingers. Hyperflexion of index finger DIPJ, hyperextension of PIPJ. Sign of RA