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1B Musculoskeletal > Introduction to Rheumatology > Flashcards

Introduction to Rheumatology Flashcards

1
Q

what does rheumatology deal with?

A

diseases of MSK system including:

joint, tendons, ligaments, muscles, bones

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2
Q

what is a joint?

A

where 2 bones meet

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3
Q

what is a tendon?

A

cords of strong fibrous collagen tissue attaching muscles to bone

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4
Q

what are ligaments?

A

flexible fibrous connective tissue which connects 2 bones

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5
Q

what are the components of a synovial joint?

A

synovium

synovial fluid

articular cartilage

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6
Q

what is the synovium?

A

1-3 cell deep lining containing macrophage-like phagocytic cells (type A synoviocytes) and fibroblast like cells that produce hyaluronic acid (type B synoviocyte)

type 1 collagen

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7
Q

what is synovial fluid?

A

hyalauronic acid-rich viscous fluid

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8
Q

what is articular cartilage made up of?

A

type II collagen

proteoglycan (Aggrecan)

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9
Q

what is arthritis?

A

disease of joint

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10
Q

what are the divisions of arthritis?

A

osteoarthritis (degenerative arthritis)

inflammatory arthritis (main type is rheumatoid arthritis_

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11
Q

what is inflammation?

A

physiological response to deal with injury/infection

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12
Q

what can excess/inappropriate inflammation reactions cause?

A

damage host tissue

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13
Q

what are the clinical signs of inflammation on examination?

A
  • RED (rubor)
  • Pain (dolor)
  • Hot (color)
  • Swelling (tumor)
  • ​Loss of function
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14
Q

what pathological, cellular and molecular changes occur during inflammation?

A
  • Increased blood flow
  • Migration white boood cells (leucocytes) into tissues
  • Activation/ differentiation of leucocytes
  • Cytokine production e.g TNF-alpha, IL1, IL6, IL17
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15
Q

what are the causes of joint inflammation?

A
  1. Crystal arthritis
    1. Gout
    2. Pseudogout
  2. Immune-mediated (‘autoimmunie)
    1. Rheumatoid arthritis
    2. Seronegative spondyloarthropathies
    3. Connective tissue diseases
  3. Infection
    1. Septic arthritis
    2. TB
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16
Q

what is gout caused by?

A

deposition of urate (uric acid) crystals -> inflammation

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17
Q

what is a risk factor for gout?

A

high levels uric acid (hyperuricaemia)

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18
Q

what are the causes of hyperuricaemia?

A
  • Genetic tendency
  • Increased intake of purine-rich foods
  • Reduced excretion (kidney failure)
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19
Q

what is acute gout?

A

Disease in which tissue deposition of monosodium urate (MSU) crystals occur as a result of hyperuricaemia and leads to:

gouty arthritis

tophi

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20
Q

what are tophi?

A

aggregated deposits of MSU in tissue

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21
Q

what does gouty arthritis commonly affect?

A

metatarsophalangeal joint of the big toe (1s MTP joint)

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22
Q

what are the signs of gouty arthritis?

A
  • podagra
  • Abrupt onset
  • Extremely painful
  • Joint red, warm, swollen and tender
  • Resolves spontaneously over 3-10 days
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23
Q

what does an X-ray of gouty arthritis show?

A

juxta-articular rate bite erosions at the MTPJ of great toe

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24
Q

what are the investigations for gout?

A

joint aspiration- synovial fluid analysis

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25
Q

what is the management of gout?

A
  • Acute attach- colcichine, NSAIDS, steroids
  • Chronic- allopurinol
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26
Q

what is pseudogout?

A
  • Pseudogout is a syndrome caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystal deposition crystals -> inflammation
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27
Q

what are the risk factors for pseudogout?

A
  • background osteoarthritis,
  • elderly patients,
    • intercurrent infection
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28
Q

what is the difference in the synovial fluid of gout and pseudogout?

A
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29
Q

what is the most common form of immune mediated inflammatory joint disease?

A

rheumatoid arthritis

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30
Q

what is 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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31
Q

what is the pathogenesis of RA?

A
  • Synovial membrane is abnormal in rheumatoid arthritis:
  • The synovium becomes a proliferated mass of tissue (pannus) due to:
    • Neovascularisation
    • Lymphangiogenesis
    • inflammatory cells:
      • activated B and T cells
      • plasma cells
      • mast cells
      • activated macrophages
  • Recruitment, activation and effector functions of these cells is controlled by a cytokine network
  • There is an excess of pro-inflammatory vs. anti-inflammatory cytokines (‘cytokine imbalance

’

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32
Q

what is a healthy synovial membrane composition?

A
  • 1 to 3 cell layer that lines synovial joints
  • Contains macrophage-like (type A synoviocyte) and fibroblast-like (type B synoviocyte) cells and type I collagen
  • Functions include the maintenance of synovial fluid, the hyaluronate-rich viscous fluid within joint space
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33
Q

what is the dominant cytokine in RA?

A

TNF-alpha

34
Q

what are the effects of TNF-alpha?

A
35
Q

how is TNF-alpha role in RA treated?

A
  • TNFα inhibition is achieved through parenteral administration (most commonly sub-cutaneous injection) of antibodies or fusion proteins
36
Q

what are the features of rheumatoid arthritis?

A
  • Chronic arthritis
    • Polyarthritis - swelling of the small joints of the hand and wrists is common
    • Symmetrical
    • Early morning stiffness in and around joints
    • May lead to joint damage and destruction - ‘joint erosions’ on radiographs
  • Extra-articular disease can occur
    • Rheumatoid nodules
    • Others rare e.g. vasculitis, episcleritis
  • Rheumatoid ‘factor’ may be detected in blood
    • Autoantibody against IgG
37
Q

what are the patterns of joint involvement in rheumatoid arthritis?

A

symmetrical

affects multiple joints (Polyarthritis) >5

affects small and large joints, particularly hands and feet

38
Q

what are the most commonly affected joints in RA?

A
  • Metacarpophalangeal joints (MCP)
  • Proximal interphalangeal joints (PIP)
  • Wrists
  • Knees
  • Ankles
  • Metatarsophalangeal joints (MTP)
39
Q

what is the primary site of pathology in rheumatoid arthritis?

A

synovium

40
Q

what are the common synovium inflammation pathologies?

A
41
Q

what are the common extra-articular features in RA?

A
  • Fever, weight loss
  • Subcutaneous nodules
42
Q

what are the uncommon extra-articular features of RA?

A
  • vasculitis
  • Ocular inflammation e.g. episcleritis
  • Neuropathies
  • Amyloidosis
  • Lung disease – nodules, fibrosis, pleuritis
  • Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis
43
Q

what are RA subcutaneous nodules?

A
  • Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue
  • Occur in ~30% of patients
44
Q

what are RA subcutaneous nodules associated with?

A

severe disease

extra-articular manifestations

rheumatoid factor

45
Q

what are the 2 types of antibodies in RA?

A

rheumatoid factor

antibodies to citrullinated protein antigens (ACPA)

46
Q

what is rheumatoid factor?

A
  1. Antibodies that recognize the Fc portion of IgG as their target antigen
  2. typically IgM antibodies i.e. IgM anti-IgG antibody !
  3. Positive in 70% at disease onset and further 10-15% become positive over the first 2 years of diagnosis
47
Q

what are ACPA?

A
  1. Antibodies to citrullinated peptides are highly specific for rheumatoid arthritis
    1. Anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’
48
Q

what enzymes is citrullination of peptides mediated by?

A
  1. Peptidyl arginine deiminases (PADs)
49
Q

what is the treatment goal of RA?

A

prevent joint damage

50
Q

what does preventing joint damage in RA require?

A
  • Early recognition of symptoms, referral and diagnosis
  • Prompt initiation of treatment: joint destruction = inflammation x time
  • Aggressive treatment to suppress inflammation
51
Q

what are the drug treatments for rheumatoid arthritis?

A
  • Disease-modifying anti-rheumatic drugs (‘DMARDs’) = drugs that control the disease process
  • 1st line treatment:
    • methotrexate in combination with hydroxychloroquine or sulfasalazine
  • 2nd line:
    • Biological therapies offer potent and targeted treatment strategies
  • New therapies include Janus Kinase inhibitors : Tofacitinib & Baricitinib
52
Q

what drug is important in RA treatment but avoided in long term use?

A

glucocorticoid therapy (prednisolone)- avoided long term due to side effects

53
Q

what multidisciplinary management can be used in RA?

A

physiotherapy, occupational therapy, hydrotherapy, surgery

54
Q

what is biologic therapy?

A
  • are proteins (usually antibodies) that specifically target a protein such as an inflammatory cytokine
55
Q

what are the types of biologics in RA?

A
  • Inhibition of tumour necrosis factor-alpha (‘anti-TNF’)
    • antibodies (infliximab, and others)
    • fusion proteins (etanercept)
  • B cell depletion
    • Rituximab – antibody against the B cell antigen, CD20
  • Modulation of T cell co-stimulation
    • Abatacept - fusion protein - extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to modified Fc (hinge, CH2, and CH3 domains) of human immunoglobulin G1
  • Inhibition of interleukin-6 signalling
    • Tocilizumab (RoActemra) – antibody against interleukin-6 receptor.
    • Sarilumab (Kevzara) – antibody against interleukin-6 receptor.
56
Q

what is the difference between osteoarthritis and RA?

A
  • Destruction joints at distal joints rather than MCP joints in RA
  • Deformity also present in RA
  • RA may have osteopenia or bony erosions
57
Q

what other conditions can cause inflammatory arthritis?

A
  1. Ankylosing spondylitis
  2. Psoriatic arthritis
  3. Reactive arthritis
  4. Systemic lupus erythematous (SLE)
58
Q

what is the demographic for ankylosing spondylitis?

A

20-30 yrs, Male

59
Q

what is ankylosing spondylitis?

A
  • Seronegative spondyloarthropathy – no positive autoantibodies
  • Chronic sacroillitis – inflammation of sacroiliac joints
  • Results in spinal fusion – ankylosis
60
Q

what is ankylosing spondylitis associated with?

A

HLA B27

61
Q

what is the clinical presentation of ankylosing spondylitis?

A
  • Lower back pain + stiffness
    • Early morning
    • Improves with exercise
  • Reduced spinal movement
  • Peripheral arthritis
  • Plantar fasciitis, Achilles tendonitis
  • Fatigue
62
Q

what are the bloods in ankylosing spondylitis?

A
  • Normocytic anaemia
  • Raised CRP, ESR
  • HLA-B27
63
Q

what imaging is taken in ankylosing spondylitis and what signs are seen?

A
  • X-Ray
  • MRI
  • Squaring Vertebral bodies, Romanus lesion
  • Erosion, sclerosis, narrowing SIJ
  • Bamboo Spine
  • Bone Marrow Oedema
64
Q

what is the management for ankylosing spondylitis?

A
  • Physiotherapy
  • Exercise regimes
  • NSAIDs
  • Peripheral joint disease – DMARDs (don’t work for spinal inflammation)
65
Q

what is psoriatic arthritis?

A
  • Psoriasis is an autoimmune disease affecting the skin (scaly red plaques on extensor surfaces eg elbows and knees)
  • ~10% of psoriasis patients also have joint inflammation
66
Q

what is the difference between RA and psoriatic arthritis?

A
  • Unlike RA, rheumatoid factors are not present (“seronegative”)
  • Varied clinical presentations (PA):
    • Classically asymmetrical arthritis affecting IPJs
67
Q

what can psoriatic arthritis manifest as?

A
  • Symmetrical involvement of small joints (rheumatoid pattern)
  • Spinal and sacroiliac joint inflammation
  • Oligoarthritis of large joints
  • Arthritis mutilans
68
Q

what are the investigations for psoriatic arthritis?

A
  • X-rays of affected joints – pencil in cup abnormality
  • MRI – sacroiliitis and enthesitis
  • Bloods – no antibodies as seronegative
69
Q

what is the managemet for psoriatic arthritis?

A
  • DMARDs – methotrexate
  • Avoid oral steroids – risk of pustular psoriasis due to skin lesions
70
Q

what is reactive arthritis?

A
  • Sterile inflammation in joints following infection especially urogenital (e.g. Chlamydia trachomatis) and gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections) infections
71
Q

what are the extra-articular manifestations of reactive arthritis?

A
  • Important extra-articular manifestations include:
    • Enthesitis (tendon inflammation)
    • Skin inflammation
    • Eye inflammation
72
Q

what might reactive arthritis be first manifestation of?

A

may be first manifestation of HIV or hepatitis C infection

73
Q

who is reactive arthritis common in?

A
  • Commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection)
74
Q

when do the symptoms start in reactive arthritis?

A

symptoms follow 1-4 weeks after infection and this infection may be mild

75
Q

how can reactive arthritis be managed?

A

Condition is usually self-limiting – can be managed with NSAIDS or DMARDs if required

76
Q

what is lupus?

A

Lupus = a multi-system autoimmune disease

Multi-site inflammation: can affect any almost any organ. (Often joints, skin, kidneys, haematology. Also: lungs, CNS involvement)

77
Q

what is systemic lupus erythematosus associated with?

A
  • Associated with antibodies to self antigens (‘autoantibodies’)
  • Autoantibodies are directed against components of the cell nucleus (nucleic acids and proteins)
78
Q

what can be a useful diagnostic in SLE?

A

autoantibodies:

  1. Antinuclear antibodies (ANA):
  • High sensitivity for SLE but not specific.
  • A negative test rules out SLE, but a positive test does not mean SLE.
  1. Anti-double stranded DNA antibodies (anti-dsDNA Abs):
    * High specificity for SLE in the context of the appropriate clinical signs.
79
Q

what is a typical sign of SLE?

A

molar/ butterfly rash

80
Q

what is the epidemiology of SLE?

A
  • F:M ratio 9:1
  • Presentation 15 - 40 yrs
  • Increased prevalence in African and Asian ancestry populations

1B Musculoskeletal (7 decks)

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