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Musculoskeletal Y2 > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

RHEUMATOID ARTHRITIS is….

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

Why can’t RA cause back pain

A

the back has no synovia

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3
Q

3 key features of RA?

A

CHRONIC ARTHRITIS
EXTRA-ARTICULAR DISEASE CAN OCCUR
RHEUMATOID ‘FACTOR’ MAY BE DETECTED IN THE BLOOD

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4
Q

Examples of synovial joints?

A
  • Metacarpophalangeal joints (MCP)
  • Proximal interphalangeal joints (PIP)
  • Wrists
  • Knees
  • Anles
  • Metatarsophalangeal joints (MTP)
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5
Q

Key features of chronic arthritis in RA? (5)

A
  • Polyarthritis- swelling of the small joints of the hand and wrists s common
  • Symmetrical
  • Early morning stiffness around joints
  • May lead to joint damage and destruction- ‘joint erosions’ or radiographs
    o Patients tend to feel ‘unwell’ as it’s a systemic illness
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6
Q

What is rheumatoid factor?

A
  • IgM autoantibody against IgG
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7
Q

What is extra-articular disease and how do these occur?

A
  • Rheumatoid nodules - subcutaneous swelling that occur in certain places which are related to rheumatoid factor and immune complexes that form
  • Others rare e.g. vasculitis, episcleritis

o This is because of rheumatoid factor (autoantibody) forming immune complexes, which can go anywhere

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8
Q

RA is more common in males or females?

A

Females

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9
Q

what is a shared epitope

A

specific set of amino acids is conserved among all HLA subtypes that are associated with RA

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10
Q

Important environmental factor in RA?

A

Smoking

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11
Q

What does synovitis to cause damage

A

Synovitis causes joint damage by damaging articular cartilage

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12
Q

What is the Swan-neck Deformity

A

o Hyperextension at the PIP

o Hyperflexion at the DIP

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13
Q

What is the Boutonniere Deformity

A

o Hyperflexion at the PIP

o Boutonniere means ‘button-like’

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14
Q

What deformity is:

o Hyperflexion at the PIP

A

Boutonniere Deformity

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15
Q

What deformity is:
o Hyperextension at the PIP
o Hyperflexion at the DIP

A

Swan-neck Deformity

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16
Q

3 sites of pathology of the synovium kn RA?

A
  1. Synovial joints
  2. Tenosynovium surrounding tnedons
  3. Bursa
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17
Q

What is SUB-CUTANEOUS NODULES? Incidence?

A
  • Central area of fibrinoid necrosis surrounded by histocytes and peripheral layer of connective tissue
  • Occur in 30% of patients
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18
Q

Rheumatoid factor is fundamentally what and most commonly how does this manifest?

A
  • Antibodies that recognise the Fc portion of IgG as their target antigen
  • Typically, IgM antibodies i.e. IgM anti-IgG antibody
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19
Q

What antibodies are highly specific for RA?

A

ANTIBODIES TO cyclic CITRULLINATED PROTEIN ANTIGENS (ACPA) (ACCP antibodies)

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20
Q

What is the tenosynovium

A

wraps around tendons to allow them to move freely

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21
Q

if rheumatoid nodules are present, then the patient is always XX positive

A

rheumatoid factor

22
Q

Why is the fact that its IgM producing autoantibodies key to producing nodules

A

Because its a pentameric Ig

23
Q

Citrullination of peptides is mediated by enzymes termed….

A
  • PEPTIDYL ARGININE DEIMINASES
24
Q

Where are peptides citrullinated

A

Frequently in areas of inflammation

25
Q

Why do multiple HLA serotypes predispose to RA?

A

Because they all contain the shared epitope, the shared 67aa long chain in their antigen binding group

26
Q

HLA serotypes associated with RA? (4)

A

HLA-DR1, HLA-DR6, HLA-DR10 as well as the HLA-DR4.

27
Q

Common extraarticular features of RA? (2)

A
  • Fever, weight loss

- Subcutaneous nodules

28
Q

Uncommon extraarticular features of RA? (6)

A
  • Vasculitis
  • Ocular inflammation e.g. episcleritis
  • Neuropathies
  • Amyloidosis
  • Lung disease- nodules, fibrosis, pleuritic
  • Felty’s syndrome- triad of splenomegaly, leukopenia and RA
29
Q

RADIOGRAPHIC ABNORMALITIES IN EARLY RA?

A

Juxta-articular osteopenia

30
Q

RADIOGRAPHIC ABNORMALITIES IN LATE RA?

A

Joint erosions at margins of the joint

31
Q

RADIOGRAPHIC ABNORMALITIES IN LATEST RA?

A

Joint deformity and destruction

32
Q

Thickness of the synovium?

A

1-3 cells deep

33
Q

Main molecule in the synovium lining?

A

Type 1 collagen

34
Q

What produces synovial fluid

A

Fibroblasts

35
Q

What cells are within the synovial lining? (2)

A

Macrophages and fibroblasts

36
Q

What molecule is in synovial fluid? What is thickness of the synovial fluid?

A

Hyaluronic acid

Viscous

37
Q

What is the articular cartilage made of?

A

T2 collagen

Aggrecan (proteoglycan)

38
Q

What is a pannus

A

proliferated mass of tissue

39
Q

What is the pathogenesis of RA? (2, 1st can be split into 3)

A

Synovial membrane is abnormal
The synovium becomes a proliferated mass of tissue (PANNUS) due to:
- Neovascularisation
- Lymphangiogenesis
- Inflammatory cells e.g. activated T and B cells, plasma cells, mast cells and activated macrophages

Recruitment, activation and effector functions of these cells is controlled by a cytokine network- there are more pro-inflammatory cytokines than anti-inflammatory (cytokine imbalance)

40
Q

• The key cytokines involved in RA are…

A

o TNFalpha, IL-1, IL-6

41
Q

• TNF-alpha is mainly produced by….

A

activated macrophages

42
Q

Best form of antibody treatment for RA patients? another 3?

A

Anti-TNFalpha
Anti IL6 is next best then Anti IL1
B cells in RA can also be depleted by parenteral (IV) administration of an AB against a B cell surface antigen- CD20.

43
Q

2 approaches in managing RA?

A

MDT approach

Medication

44
Q

Drugs that are used to treat RA? (4)

A

Disease modifying anti-rheumatic drugs (DMARDs)
Biological therapies

glucocorticoids

45
Q

DMARD THERAPY aims to achieve what (2)

A
  1. Reducing synovial inflammation

2. Slowing/preventing structural joint damage e.g. bone erosions

46
Q

Onset of DMARDs?

A

Slow onset of action e.g. weeks

47
Q

Example of DMARD?

A
  • METHOTREXATE or

JANUS KINASE INHIBITORS

48
Q

4 biologic therapies for RA?

A

INHIBITION OF TNF-ALPHA (ANTI-TNF)
B CELL DEPLETION
3. MODULATION OF T CELL CO-STIMULATION
4. INHIBITION OF IL-6

49
Q

Anti-TNFalpha antibody name?

A

infliximab

50
Q

Downside to biological therapy? (2)

A

ll expensive so in England their use follows NICE guidelines

Side-effects for all include increased infection risk

Musculoskeletal Y2 (11 decks)

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