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Y2 LCRS 2 - NMH, Psych, Anatomy of Limbs, Head, Neck & Spine, Musculoskeletal > MSK; Lecture 4, 5 and 6 - Pathogenesis of AI disease, Rheumatoid Arthritis and Osteoarthritis/Reactive arthritis > Flashcards

MSK; Lecture 4, 5 and 6 - Pathogenesis of AI disease, Rheumatoid Arthritis and Osteoarthritis/Reactive arthritis Flashcards

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1
Q

What is rheumatoid arthritis?

A

Chronic joint inflammation that can result in joint damage (permanent) -> synovium is inflammed; associated with autoantibodies

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2
Q

Which autoantibodies are associated with rheumatoid arthritis?

A

Rheumatoid factor and anti-cyclic citrullinated peptide (anti-CCP)

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3
Q

What is ankylosing spondylitis?

A

Chronic spinal inflammation that can result in spinal fusion and deformity -> chronic back pain from enthesis (site of inflammation - junction between intervertebral disc and vertebrae); no autoantibodies.

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4
Q

What are seronegative spondyloarthropathies?

A

Ankylosing spondylitis; reiters syndrome and reactive arthritis. Arthritis associated with psoriasis (psoriatic arthritis)/GI inflammation (IBS - enteropathic synovitis)

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5
Q

What are the signs of the patient with ankylosing spondylitis?

A

Excessive thoracic kyphosis; no lordosis in lumbar spine and hyperextension of neck -> spine moves as a block

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6
Q

What is SLE?

A

Chronic tissue inflammation in presence of Ab direted against self-Ag; multi-site inflammation, particularly joints, skin and kidneys -> excessive immune complexes which deposit in tissues, but have low complement levels Associated with autoAb

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7
Q

Which autoAb is SLE associated with?

A

Antinuclear Ab and anti-double stranded DNA ab

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8
Q

What are the different connective tissue diseases?

A

Systemic lupus erythematosus Inflammatory muscle disease: polymyositis, dermatomyositis Systemic sclerosis Sjogren’s syndrome A mixture of the above: ‘Overlap syndromes’

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9
Q

Which HLA molecules are associated with rheumatoid arthritis, SLE and ankylosing spondylitis?

A

RA = HLA-DR4 (class II) SLE = HLA-DR3 (class II) AS = HLA-B27 (class I)

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10
Q

What is the importance of the MHC being class I or II?

A
  • Presents ag to T-cells.
  • Pathogenesis of HLA-associated disease -> due to a peptide antigen (exogenous or self) that is able to bind to HLA molecule and trigger disease (‘arthritogenic antigen’)
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11
Q

What are the overall autoantibodies used in rheumatology (RA, SLE, osteoarthritis, reactive arthritis, gout, AS, systemic vasculitis)?

A
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12
Q

What are the autoantibodies in diffuse/limited systemic sclerosis, dermato-polymitosis, sjogren’s syndrome, mixed connective tissue disease?

A
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13
Q

What are the autoantibodies of SLE?

A

NB: antinuclear antibodies do not enter the nucleus/cell; the nuclear antigens are presented by the cell via HLA receptor (e.g.)

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14
Q

What are antinuclear antibodies reacting to?

A

If ANA is positive the clinical laboratory will perform further tests to determine which type of ANA it is – typically these include screening for: Anti-Ro Anti-La Anti-centromere Anti-Sm Anti-RNP Anti-ds-DNA antibodies Anti-Scl-70 Cytoplasmic antibodies include: Anti-tRNA synthetase antibodies Anti-ribosomal P antibodies

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15
Q

How is the disease activity of SLE worked out?

A

Sick lupus patients have low complement levels and high levels of anti-ds-DNA Ab, which cycles

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16
Q

What are the cytokines used in rheumatology and what are their effects?

A

TNF-a is very beneficial as it is the main inflammatory mediator, so by inhibiting it helps greatly reduce the inflammation

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17
Q

How does TNF-a act in rheumatoid arthritis?

A

TNF-a is very beneficial as it is the main inflammatory mediator, so by inhibiting it helps greatly reduce the inflammation -> reduces cartilage damage and joint inflammation

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18
Q

What other cytokine inhibitors are present in clinic for rheumatoid conditions?

A

IL-6 and IL-1 blockade are now available in clinic; can also deplete B cells in rheumatoid arthritis by parenteral admin of Ab against CD20

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19
Q

How is RANKL used in rheumatology?

A
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20
Q

How can B cells inhibitors be used to treat SLE?

A
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21
Q

How are prostaglandins used in rheumatology?

A

See them as anti-iinflammatory and analgesic -> don’t modify joint destruction, just manages the pain not stopping the disease

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22
Q

What is rheumatoid arthritis?

A

Chronic AI disease characterised by pain, joint stiffness and SYMMETRICAL synovitis of synovial joints (needs to be on both sides of body)

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23
Q

What are the environmental/genetic components of rheumatoid arthritis?

A
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24
Q

What are the commonest affected joints in rheumatoid arthritis?

A

MCP, Proximal interphalangeal joints, wrists, knees, ankles, MTP

25
Q

What are the types of joint damage and destruction that occurs in rheumatoid arthritis?

A

Swan-neck deformity and boutonniere deformity

26
Q

What are the types of synovitis that can appear and where?

A
27
Q

What are sub-cutaneous nodules that can present in rheumatoid arthritis?

A

Histiocytes surrounded by connective tissue

28
Q

What is the importance of Ab to citrullinated protein antigens?

A
29
Q

What is the pathology of rheumatoid arthritis?

A

Peri-osteus inflammation; articular cartilage is lost

30
Q

What are the features of the synovial joint?

A

Synovium, synovial fluid and articular cartilage (type II collagen - bONE has type I

31
Q

How is synovial fluid abnormal in rheumatoid arthritis?

A
32
Q

How is TNF-a important in rheumatoid arthritis and how can we use this for treatment?

A

Dominant detrimental role of TNFα in rheumatoid arthritis validated by the therapeutic success of TNFα inhibition in this condition. TNFα inhibition is achieved through parenteral administration (most commonly sub-cutaneous injection) of antibodies or fusion proteins

33
Q

What are the biological therapies for rheumatoid arthritis?

A
34
Q

What are the treatment goals and general treatments for rheumatoid arthritis?

A

Methotrexate is the main drug given to patients. Think of side effect profiles for long standing treatment

35
Q

What are DMARDS?

A
36
Q

What are the negatives of biological therapy for rheumatoid arthritis?

A
37
Q

What is reactive arthritis?

A
38
Q

How can you differentiate the musculoskeletal symptoms of reactive arthritis from enthesitis and spondylitis?

A

Can present as monoarthritis

39
Q

What are the extra-articular features of reactive arthritis?

A

NB: reiter’s syndrome is the same thing as reactive arthritis

40
Q

What is the difference between rheumatoid and reactive arthritis?

A

K. blennorhagicum (psoriasis-like rash in feet). NB: NO Ab in reactive

41
Q

*What is osteoarthritis?

A

Chronic slowly progressive disorder due to failure of articular cartilage that typically affecting joints of the hand (especially those involved in pinch grip), spine and weight-bearing joints (hips and knees)

42
Q

Which joints are affected in osteoarthritis?

A

Joints of hand -> DIP, PIP and CMC (not MCP); spine and weight bearing joints of lower limbs -> hip, knees and MTP

43
Q

What are some physical features of osteoarthritis?

A

x

44
Q

What features can osteoarthritis be associated with?

A

x

45
Q

What are the radiographic features of osteoarthritis?

A

Joint space narrowing Subchondral bony sclerosis Osteophytes Subchondral cysts

46
Q

What is the pathology for osteoarthritis?

A

Defective and irreversible articular cartilage an damage to underlying bone -> develops due to excessive loading on joints and/or abnormal joint components

47
Q

What are proteoglycans?

A

Aggrecan is the major proteoglycan in articular cartilage Hyaluronic acid is the only non-sulphated GAG and is major component of synovial fluid where it has an important role in maintaining synovial fluid viscosity

48
Q

How do you manage osteoarthritis?

A

Mainly to improve pain management, not real treatment

49
Q

What is Belimumab?

A

Recombinant fully human IgG1 mAb against BLYS -> inhibits activity of BAFF resulting in impaired B cell survival and reduced B cell numbers

50
Q

What is rheumatoid factor?

A
51
Q

What are the extra-articular features of rheumatoid arthritis?

A
52
Q

What are the radiographic abnormalities of rheumatoid arthritis at different progressions?

A

x

53
Q

How do you diagnose reactive arthritis?

A
54
Q

What is the difference between septic vs reactive arthritis?

A
55
Q

How do you treat reactive arthritis?

A
56
Q

What are the radiographic changes in rheumatoid arthritis vs osteoarthritis?

A
57
Q

How is the articular cartilage different in osteoarthritis?

A
58
Q

What are the cartilage and bone changes in osteoarthritis?

A
59
Q

How do you treat osteoarthritis?

A

Y2 LCRS 2 - NMH, Psych, Anatomy of Limbs, Head, Neck & Spine, Musculoskeletal (17 decks)

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