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eLCRS - 머크 > 2 Rheumatology - Rheumatoid Arthritis > Flashcards

2 Rheumatology - Rheumatoid Arthritis Flashcards

1
Q

Define 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 key features of chronic arthritis?

  • is it symmetrical/asymmetrical?
  • what time of the day?
  • what might be seen on radiographs?
A
  • Polyarthritis - swelling of the small joints of the hand and wrists is common
  • Symmetrical
  • Early morning stiffness in + around joints (marker for treatment)
  • May lead to joint damage and destruction - ‘joint erosions’ on radiographs
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3
Q

What rheumatoid factor might be found in blood if you have rheumatoid arthritis ?

A

IgM autoantibody against IgG

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4
Q

in terms of genes,

what gene variants are strongly associated with rheumatoid arthritis?

A

HLA-DRB gene variants mapping to amino acids 70-74 of the DRb-chains = strongly associated with rheumatoid arthritis

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5
Q

what environmental factor can contribute to arthritis?

A

smoking

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6
Q

What are the commonest affected joints in rheumatoid arthritis?

A
  • Metacarpophalangeal joints (MCP)
  • Proximal interphalangeal joints (PIP)
  • Wrists
  • Knees
  • Ankles
  • Metatarsophalangeal joints (MTP)
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7
Q

What is characteristic of Joint Damage and Destruction in rheumatoid arthritis?

damage to: _____ _______

A

damages articular cartilage

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8
Q

What is Swan-neck Deformity in RA

A

o Hyperextension at PIP

o Hyperflexion at DIP

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9
Q

What is Boutonniere Deformity in RA

A

Hyperflexion at PIP

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10
Q

why might you get deformity of joints in RA?

A

Synovitis has damaged joints, so surrounding tendons are pulling on abnormal joint –> causes deformity

  • -> joints are not aligned
  • -> joints are eroded
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11
Q

primary site of pathology of RA is in the _____ which includes

  • synovial joints
  • Tenosynovium surrounding tendons
  • Bursa
A

primary site of pathology of RA is in the Synovium which includes

  • synovial joints (synovitis)
  • Tenosynovium surrounding tendons (tenosynovitis)
  • Bursa (bursitis)
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12
Q

Sub-cutaneous nodules may present in patients with RA

what is Sub-cutaneous nodules?

A
  • when Central area of fibrinoid necrosis = surrounded by histiocytes and peripheral layer of connective tissue
  • -> typically presents in ulnar border of forearm
note:
Associated with
- Severe disease
- Extra-articular manifestations
- Rheumatoid factor
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13
Q

What are rheumatoid factors?

A
  • Antibodies that recognize the Fc portion of IgG as their target antigen
  • typically IgM antibodies i.e. IgM anti-IgG antibody
  • usually positive for RA
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14
Q

Antibodies to Citrullinated Protein Antigens (ACPA/CCP): highly specific for RA

what are they mediated by?

A

Citrullination of peptides mediated by peptidyl arginine deiminases (PADs)

arginine = converted to –> citrulline (via PADs)

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15
Q

NOTE: peptidyl arginine deiminases PADs found in high conc. in neutrophils + monocytes –> common in inflamed sites e.g. synovium

  • ACPA strongly associated with smoking + HLA ‘shared epitope’
A
  • chronic inflammation –> increase in inflammation + citrullination
    causes e.g smoking/ gingivitis
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16
Q

What are some Extra-articular features of RA?

A

Common:

  • Fever
  • weight loss
  • malaise, lethargy (driven by cytokines)
  • Subcutaneous nodules

Uncommon:

  • vasculitis
  • Ocular inflammation e.g. episcleritis
  • Neuropathies
  • Amyloidosis
  • Lung disease
  • Felty’s syndrome
17
Q

What are Radiographic abnormalities you might find in a patient with RA at

a) early stages
b) Later
c) Later still

A

Early= Juxta-articular osteopenia

Later= Joint erosions at margins of the joint

Later still= Joint deformity and destruction

18
Q

Describe the pathology of RA.

A

Normally, synovium contacting bone = NOT articular cartilage
–> so there’s small space of bone in synovium not covered by articular cartilage (bare area)

  • In synovitis, articular cartilage = susceptible to damage by inflammation –> see erosion first at bare area + edges of articular cartilage
  • Can also see joint space narrowing –> less articular cartilage –> bones come closer
    i. e synovitis, bone erosion, cartilage degradation
19
Q

Synovium = made up of _______

A

synoviocytes

20
Q

describe the composition of Synovial joint

A
  • 1-3 cell deep lining containing type A synoviocyte + type B synoviocyte
  • Type I collagen
21
Q

Describe the pathogenesis of RA

A

Synovium becomes a proliferated mass of tissue (pannus) due to:

o Neovascularisation - formation of new blood vessels

o Lymphangiogenesis - formation of new lymphatics

o Many inflammatory cell

o cytokine imbalance

22
Q

What are some methods of biological therapy against RA?

A
  • interleukin-6 + interleukin-1 blockade
  • anti-TNF
  • deplete B cells
  • -> (intravenous) administration of an antibody against a B cell surface antigen, CD20
  • -> rituximab
  • Modulation of T cell co-stimulation
23
Q

Management of RA

A
  • multidisciplinary approach (physiotherapy/ occupational therapy etc.)
  • DMARDs
  • Glucocorticoid therapy
  • Biological therapies
24
Q

What is DMARD Therapy?

A

drugs that may induce remission (not cure) and prevent joint damage

by:
- reducing the amount of inflammation in the synovium
- slow/ prevent structural joint damage e.g. bone erosions

25
Q

What are some e.g of drugs used in DMARD Therapy?

A

a) methotrexate – common
b) sulphasalazine – common
c) hydroxychloroquine – common
d) leflunomide – uncommon
e) Janus Kinase inhibitors

ALL = blood test monitored every 6-8wks

26
Q

What are downsides of biological therapy against RA?

A
  • expensive
  • side effect = increases infection risk
  • TNF-a inhibition = associated w increased susceptibility to mycobacterial infection –> can cause tuberculosis
  • B cell depletion therapy = linked with hep B reactivation

eLCRS - 머크 (9 decks)

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