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Year 2 BRS added > Rheumatoid and Other Inflammatory Arthritis > Flashcards

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
Q

Healthy synovial membrane?

A

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
Q

Synovial membrane in RA?

A

Synovium becomes a proliferated mass of tissue (pannus) due to:
Neovascularisation
Lymphangiogenesis
Inflammatory cells

27
Q

Which inflammatory cells cause synovium to become proliferated mass of tissue?

A

Activated B and T cells
Plasma cells
Mast cells
Activated macrophages

28
Q

Pannus?

A

Proliferated mass of tissue

29
Q

RA pathogenesis with treatments? B, T and cytokines

A
  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
Q

TNF-alpha in RA?

A

Dominant pro-inflammatory cytokine in rheumatoid synovium

31
Q

TNF-a actions in RA?

A

Inflammatory cell recruitment, angiogenesis, lymphangiogenesis -> pannus formation

Matrix metalloproteases -> cartilage loss

Osteoclast activation -> bone loss

32
Q

RA bloods?

A

Increased ESR, CRP
Sometimes normocytic anaemia, increased PLT

Rheumatoid factor, anti-CCP antibodies

33
Q

RA autoantibodies?

A

Rheumatoid factor - binds IgG, can be positive in other conditions
Anti-CCP antibodies - most specific, suggest more aggressive/erosive disease

34
Q

RA steps to symptoms?

A

Genetic predisposition -> pre-clinical autoimmunity -> tissue inflammation and disease (symptomatic)

RF and ACPAs precede symptom onset

35
Q

Radiographic features of RA? X-rays

A

Soft tissue swelling
Peri-articular osteopenia
Bone erosions

36
Q

RA ultrasound signs?

A

Synovial thickening (synovial hypertrophy)
Increased blood flow (Doppler signal)
Erosions

much better at detecting synovitis

37
Q

DMARDs?

A

Disease-modifying anti-rheumatic drugs
Immunomodulatory drugs that halt or slow the disease process

38
Q

RA first line pharmacological treatment?

A

Combination of DMARD therapy:
Methotrexate + hydroxychloroquine and/or sulfasalazine
PLUS
Steroids

39
Q

RA second line pharmacological treatment?

A

Biological therapies (usually therapeutic monoclonal antibodies) e.g. TNF-alpha blockade

40
Q

Glucocorticoids MOA?

A

Bind glucocorticoid receptor (in cytoplasm)
Steroid-GR complex translocates to nucleus and binds DNA response elements, affecting transcription

41
Q

DAS28 score?

A

Used to calculate disease
Includes number of tender joints, number of swollen joints, visual analogue score, and ESR (or CRP)

42
Q

Biological therapies targeting cytokines?

A
  1. Anti-TNF - Infliximab, adalimumab
  2. Anti-IL6 (tocilizumab)
43
Q

Biological therapies targeting lymphocytes?

A
  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
Q

Seronegative arthritis examples?

A

Psoriatic arthritis
Ankylosing spondylitis
Reactive arthritis

45
Q

Seronegative arthritis autoantibodies?

A

None present. NO anti-CCP nor RF.

46
Q

Psoriatic arthritis?

A

Psoriasis - immune-mediated disease affecting the skin. Scaly red plaques on extensor surfaces.
10% also have joint inflammation
Seronegative.

47
Q

Psoriatic arthritis pathogenic pathway? IL

A

IL-17/IL-23

48
Q

Psoriatic arthritis signs?

A

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
Q

Reactive arthritis?

A

Sterile inflammation in joints following infections elsewhere in body (usually after 1-4 weeks)

50
Q

Reactive arthritis common infections?

A

Urogenital (chlamydia trachomatis)
Gastrointestinal (salmonella, shigella, campylobacter)

51
Q

Reactive arthritis extra-articular manifestations?

A

Enthesitis
Skin inflammation
Eye inflammation

52
Q

Septic arthritis vs reactive arthritis synovial fluid culture?

A

Septic - positive
Reactive - negative

53
Q

Septic arthritis vs reactive arthritis antibiotic therapy?

A

Septic - yes, IV
Reactive - no, unless to treat underlying cause

54
Q

Septic arthritis vs reactive arthritis joint lavage?

A

Septic - yes
Reactive - no

55
Q

Osteoarthritis LOSS?

A

Loss of joint space
Osteophytes
Sclerosis
Subchondral cysts

56
Q

Heberden’s vs Bouchard’s?

A

Heberden’s - DIPs
Bouchard’s - PIPs

osteoarthritis

57
Q

Swan neck sign?

A

Chronic deformity of fingers. Hyperflexion of index finger DIPJ, hyperextension of PIPJ.
Sign of RA

Year 2 BRS added (13 decks)

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