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Musculoskeletal- > The Science of Rheumatoid Arthritis > Flashcards

The Science of Rheumatoid Arthritis Flashcards

1
Q

What is rheumatology?

A

Rheumatology = medial speciality that deals with patients with arthritis and other related conditions

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2
Q

What is arthritis?

A

Arthritis = inflammation of a joint

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3
Q

What is the clinical presentation of arthritis?

A
  • Symptoms
    • Pain
    • Stiffness
    • Swelling
    • Functional impairment
    • Systemic symptoms
  • Signs
    • Tenderness
    • Swelling
    • Restriction of movement
    • Heat
    • Red
    • Systemic features
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4
Q

What are examples of rheumatic diseases?

A
  • RA
  • Sero nergative arthritis
  • Crystal arthritis
  • Connective tissue diseases
  • Systemic vasculitis
  • Bone disease
  • Osteoarthritis (most prevalent kind of arthritis)
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5
Q

What does RA stand for?

A

Rheumatoid arthritis

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6
Q

What is the most prevalent kind of arthritis?

A

Osteoarthritis

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7
Q

What is rheumatoid arthritis?

A

Rheumatoid arthritis (RA) = chronic, autoimmune systemic illness characterised by a symmetrical peripheral arthritis and other systemic features

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8
Q

What can RA be associated with?

A
  • Joint damage
  • Disability
  • Premature mortality
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9
Q

Describe how RA is classified?

A

Score of 6 or above is needed for classification of patient to deffinitely have RA:

  • joint involvement
  • serology
  • acute-phase reactants
  • duraction of symptoms
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10
Q

What is the prevalence of RA?

A

1% of population

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11
Q

What sex and age group does RA mostly affect?

A
  • Females > males 3:1
  • Age groups 4th and 5th decade
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12
Q

What is the aetiology of RA?

A
  • Genetic
    • Genetic contribution estimated to be about 50%
    • Closes association with specific amino acid sequences at positions 70-74 of DRB1
  • Environment
    • Smoking
    • Chronic infection
      • Such as periodontal disease
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13
Q

Describe the pathology of RA?

A
  • Synovitis
    • Inflamed synovium
    • Inflamed joint capsule
  • Damages surrounding structures
    • Cartilage
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14
Q

What investigations are done for RA?

A
  • Immunology
    • Rheumatoid factor (IgG, IgM)
      • Not used anymore
    • Anti-cyclic citrullinated antibodies (anti CCP, ACPA)
  • Imaging
    • X-ray
    • USS
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15
Q

What antibodies are checked to diagnose RA?

A
  • Anti-cyclic citrullinated antibodies (anti CCP, ACPA)
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16
Q

What are the clinical features of RA?

A
  • Symptoms
    • Pain
    • Stiffness
    • Immobility
    • Poor function
    • Systemic symptoms
      • Nonspecific – fatigue, weight loss, anaemia
      • Specific – eyes, lungs, nerves, skin, kidneys
      • Long term – CVS, malignancy
  • Signs
    • Swelling
    • Tenderness
    • Limitation of movement
    • Redness
    • Heat
17
Q

How many joints are usually inflammed in RA?

A

With RA usually more than 1 joint is inflamed, normally bilateral (symmetrical polyarthritis)

18
Q

How is the severity of RA assessed?

A
  • Disease severity score (DAS)
    • www.das28.com
      • DAS <2.4 represents clinical remission
      • SAD >5.1 represents eligibility for biological therapy
19
Q

What does DAS stand for?

A

Disease severity score

20
Q

What is the main concern in terms of the prognosis of RA?

A
  • Massive impact on work
    • About 33% stopped working within 2 years, 50% within 10 years
    • 40 sick days per year instead of average 6.5
21
Q

What are the functions of a Synovium?

A
  • maintenance of intact tissue surface
  • lubrication of cartilage
  • control of synovial fluid volume and composition (hyaluronan, lubricin)
  • nutrition of chondrocytes within joints
22
Q

The Synovium consist of how many layers?

A

2-3 layers

  • consist of two cell types
    • Macrophages
    • fibroblast
23
Q

Definition of RA

A
  • The rheumatoid synovitis (pannus) is characterised by inflammatory cell infiltration, synoviocyte proliferation and neoangiogenesis
  • The synovial fluid in the joint cavity contains neutrophils, particularly during acute flares of RA
  • The synovial pannus causes bone and cartilage destruction (deformities)•
24
Q

What is Pannus?

A
  • Inflammation and exuberant proliferation of the synovium leads to formation of pannus and destruction of cartilage, bone, tendons, ligaments, and blood vessels.
  • Basically, the hypertrophied synovium is called pannus.
25
Q

What auto-bodies are associated with RA?

A

RFs and anti-citrullinated protein antibodies

26
Q

Can RA be detected before onset of clinical features?

A
  • Evidence of autoimmunity can be present in RA many years before the onset of clinical arthritis
  • Autoantibodies occur in RA that recognise either joint antigens, such as type II collagen, or systemic antigens, such as glucose phosphate isomerase
  • The autoantibodies potentially can contribute to inflammation through several mechanisms, including activation of complement
27
Q

How are the RA patients classified?

A
  • Seropositive rheumatoid arthritis
    • Rheumatoid factor
    • Anti-citrullinated protein antibody (ACPA)
    • Diagnostic anti-CCP assays recognise citrullinated self-proteins
    • α-enolase, keratin, fibrinogen, fibronectin, collagen, vimentin
    • Patients with ACPA+ disease have a less favourable prognosis
      • Seronegative rheumatoid arthritis
    • not detectable
28
Q

What is Seropositive Rheumatoid Arthritis?

A
  • Seropositive rheumatoid arthritis will have detectable:
    • Rheumatoid factor
    • Anti-citrullinated protein antibody (ACPA)
    • Diagnostic anti-CCP assays recognise citrullinated self-proteins
    • α-enolase, keratin, fibrinogen, fibronectin, collagen, vimentin
    • Patients with ACPA+ disease have a less favourable prognosis
      *
29
Q

What is Rheumatic Factor?

A
  • It’s an auto antibody to self IgG Fc and IgM
  • but it’s not very specific because rheumatoid factor can also be detected in other conditions, such as Sjogren’s syndrome.
30
Q

What genes plays a role in susceptibility to RA?

A
  • Several genes are implicated in susceptibility to RA and severity of disease, including class II major histocompatibility complex genes and PTPN22
  • Distinct genetic associations for ACPA-positive and ACPA-negative RA
31
Q

What are the environmental factors for RA?

A
  • Smoking and bronchial stress (exposure to silica)
  • Infectious agents have been associated with RA
    • Viruses (EBV, CMV)
    • E. Coli
    • Mycoplasma
    • Periodontal disease (Porphyromonas gingivalis)
    • Microbiome (gut microbes)
  • Repeated insults in a genetically susceptible individual would lead to–Formation of immune complexes and rheumatoid factor (high-affinity autoAb against the Fc portion of Ig)
    • Altered citrullination of proteins and breakdown of tolerance, with resulting ACPA response
32
Q

What is Citrullination?

A
  • Citrullination (or deimination) is the conversion of the amino acid arginine in a protein into the amino acid citrulline.
  • Enzymes called peptidylarginine deiminases (PADs) replace the primary ketimine group (=NH) by a ketone group (=O).
33
Q

What happens in abnormal Citrullination?

A
  • abnormal citrullination results in auto antigens to be no longer be recognised as self antigens,
  • therefore triggering an immune mediated response.
34
Q

What are the key features to be found in Synovitis?

A
  • Villous hyperplasia
  • Infiltration of T cells, B cells, macrophages and plasma cells
  • Intimal cell proliferation (fibroblasts)
  • Production of cytokines and proteases
  • Increased vascularity
  • Self-amplifying process
35
Q

What cytokines perpetuate synovial Inflammation?

A

TNF-α, IL-6, IL-1, IL-15, IL-18, IL-23 etc. perpetuate synovial inflammation

36
Q

How does Neo-angiogenesi affect RA?

A
  • Provides nutrients to the hyperplastic synovium
  • Hypoxic conditions and angiogenic factors such as IL-8 and VEGF enhance blood vessel proliferation in the synovium
  • Microvascular endothelia in the synovium express adhesion molecules that guide circulating cells into the joint under the influence of chemoattractants
  • All of this further amplify inflammation
37
Q

What is responsible for cartilage and bone destruction?

A
  • Bone- Osteoclasts
  • Cartilage- Fibroblast (releases an enzyme call metalloproteinases)

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