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Musculoskeletal > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What are the functions of the synovium?

A
  • maintenance of intact tissue surface
  • lubrication of cartilage
  • nutrition of chondrocytes within joints
  • control of synovial fluid volume and composition (hyaluronan, lubricin)
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2
Q

Define Rheumatoid Arthritis

A

a chronic, symmetrical, polyatricular inflammatory joint disease primarily affecting small joints of hands and feet

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3
Q

What are characteristics of Rheumatoid Arthritis?

A

Inflammatory cell infiltration, synoviocytes, proliferation and neoangiogenesis

Synovial fluid in joint cavity contains neutrophils especially during acute flares

Synovial pannus causes bone and cartilage destruction

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4
Q

What is pannus?

A

An abnormal layer of fibrovascular tissue or granulation tissue

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5
Q

What evidence can sometimes be found of autoimmunity in Rheumatoid Arthritis (even before onset)?

A

Autoantibodies i.e. RFs and anti-citrullinated protein antibodies

Autoantibodies can recognise joint antigens (i.e. type II collagen) or systemic antigens (i.e. glucose phospahte isomerase)

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6
Q

Describe seropositive RA

A

Most common

Blood tests positive for antibodies hypothesised to cause RA

  • Rheumatoid factor
  • Anti-citrullinated protein antibody (ACPA)
  • Diagnostic anti-Cyclic Citrullinated Peptide assays recognise citrullinated self-proteins

Patients with ACPA+ disease have less favourable prognosis

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7
Q

What does citrullinated mean?

A

A protein in which AA arginine has been converted to the AA citrulline

Enzymes called peptidylarginine deaminases replace the ketimine group (=NH) with a ketone group (=O)

The immune system recognises these causing autoimmune response

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8
Q

What is rheumatoid factor?

A

An auto antibody to self IgG Fc

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9
Q

What infectious agents have been associated with RA?

A
  • Viruses i.e. EBV, CMV
  • E. Coli
  • Mycoplasma
  • Periodontal disease (porphyromonas gingivalis)
  • Microbiome (gut microbes)
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10
Q

What is synovitis?

A

Medical term for inflammation of synovial membrane

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11
Q

Describe the pathogenesis of synovitis in RA

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

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12
Q

Describe the roll of inflammatory cytokines in RA

A

Induce expression endothelial cells adhesion molecules

Activate synovial fibroblasts, chondrocytes, osteoclasts

Promote angiogenesis

Suppress T-regs

Activate leukocytes

Promote autoAb production

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13
Q

Describe neoangiogenesis in RA

A

Provides nutrients to hyperplastic synovium

Hypoxic conditions and angiogenic factors such as IL-8 and VEGF enhance blood vessel proliferation in the synovium

MIcrovascular endothelia in synovium express adhesion molecules that guide circulating cells into joint under the influence of hemoattractants

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14
Q

Describe cartilage and bone destruction in RA

A

Distinct mechanisms and cell types regualte this process

Several classes of proteases are produced by FLS in intimal lining layer

Synovial lining cells, especially FLS can attach to and invade cartilage in RA

Bone destruction is mediated by osteoclasts activated under influence of RANKL produced by RA synovium

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15
Q

What is RANKL?

A

Receptor activator of nuclear factor kappa-B

AKA

osteoclast differentiation factor

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16
Q

Systemic consequences of RA

A

Vasculitis, nodules, scleritis, amyloidosis

CVD; altered lipid metabolism, elevated acute-phase reactants, increased endothelial activation

Fatigue and reduced cognitive function

Liver; elevate acute-phase response, anaemia/chronic disease

Lungs, muscles, bone (osteoporosis), secondary Sjogren’s syndrome

17
Q

What is Sjogren’s syndrome?

A

A condition affecting the parts of the body that produce fluid or fluid-like substances i.e. tear ducts, salivary glands

Symptoms include dry eyes, dry mouth etc.

18
Q

What are the therapeutic categories for Rheumatoid Arthritis?

A

1) NSAIDs
2) Disease Modifying anti-Rheumatic Drugs (DMARD)
3) Biologics
4) Corticosteroids (oral, IM, IA)

19
Q

What are DMARDs?

A

Disease Modifying Anti-Rheumatic Drugs

A group of structurally unrelated, small molecule drugs which have been demonstrated to have slow onset effect on disease activity and inhibit disease progression

Traditionally assoc. with identifiable toxicity profiles and risk occasional serious adverse event

20
Q

What are some DMARD drugs?

A

Methotrexate; effective, well tolerated, cheap

Sulfasalazine
Hydroxychloroquinine
Leflunomide

21
Q

What are biologic DMARDs?

A

Drugs which have been developed from understanding inflammatory cascade to target key parts

Typically large complex proteins which need to be given parenterally

Compared to traditional DMARDs they work rapidly, are well tolerated and have high cost

  • TNFalpha inhibitors
  • IL-1 inhibitors
  • anti cell b therapies
  • anti cell c therapies
  • IL-6 inhibitors
22
Q

What are some issues with biologic DMARDs?

A

Efficacy; enhanced response when co-prescribed

TOxicity; minor eg injection site reaction, infection

Cost; expensive compared to non-biologic DMARD

23
Q

Describe the use of corticosteroids in RA

A

Can be oral, IA or IM injection and by IV infusion

Short term benefit v long term toxicity

Rarely appropriate as single drug therapy

24
Q

Describe seronegative RA

A

Where blood work shows no signs

25
Q

What is Sulfasalazine?

A

DMARD used in treatment of UC and Crohn’s

It also reduces inflammation in joints thus can be used in RA

26
Q

Describe a possible stepping up process for medication in RA

A

Initiate DMARD therapy (i.e. Sulfasalazine)

Monitor in clinic, if worsening then initiate dual DMARD therapy (i.e. add methotrexate)

Further flare on dual DMARD then can assess for biologic therapy and commence (i.e. anti-TNF alpha)

27
Q

What are some orthopaedic complications of RA?

A 
Chronic synovitis
Mechanical deformities
Secondary OA
Poor function
Pain
28
Q

Describe potential extra-articular involvement in RA

A

Rheumatoid nodules
Interstitial lung disease
Vasculitis

29
Q

How can we attempt to overcome the functional impairment caused by RA?

A 
Special adaptive cutlery
Special footwear
Walking aids
Wheelchair for outdoors
Support of family
Care packages

Musculoskeletal (16 decks)

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