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Year 1 Locomotion > Rheumatoid arthritis > Flashcards

Rheumatoid arthritis Flashcards

1
Q

Name 4 sources of musculoskeletal pain

A

Soft tissue

Bone

Joint

Refered/central

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2
Q

What are the two main types of joint disorder?

Give and example of each

What is affected in these disorders?

A

Inflammatory disorders

Rheumatoid arthritis

Synovial membrane

Degenerative disorders

Osteoarthritis

Cartilage

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3
Q

Give 3 examples of autoimmune disorders

A

Rheumatoid arthritis

Connective tissue disorder

Spondylo-arthritis

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4
Q

Name some causes of inflammatory polyarthritis

A

Infection - septic arthritis

Crystal arthritis

Rheumatoid arthritis

Reactive arthritis

Sarcoidosis

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5
Q

What is the synovium?

A

Specialised layer of fibrous connective tissue that lines the inner aspect of the fibrous joint capsule and tendon sheaths

It secretes synovial fluid

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6
Q

What is the function of synovial fluid?

A

Synovial fluid acts as:

Metabolite exchange medium

Lubricant for synovial joints

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7
Q

Why does the prevalence of autoantibodies increase with advancing age?

A

One theory is that repeat exposure to infection causes an increase in autoantibodies

Everyone has autoantibodies, however autoantibodies don’t always result in autoimmune disease

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8
Q

How can autoimmune T-cells be responsible for autoimmune diseases?

A

Millions of T cells made daily in the thymic cortex

Many of these are deleted as they recognise self-peptides strongly, others do not recognise anything and die

A few recognise self-peptide weakly and are allowed to mature and leave the thymus

Autoimmune disorders can occur when there are defects in the regulatory T cells

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9
Q

Name some theories of autoimmunity

A

Defects in regulatory T cells

Molectular mimicry between pathogens and self-peptides

Polycolonal activation of B calls during immune responses or infection, leads to recognition of self antigens

Sequestered antigen not seen by developing T and B cells, so therefore seen as a foreign antigen eg. sperm

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10
Q

If everyone has autoantibodies, why dont all people have autoimmune disorders?

A

Some people are more genetically susseptible = AI disorders run in families

A person who has one AI disorder, is more susseptible to get another that a person without a AI disorder. eg. AIDS

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11
Q

Name 2 factors that can increase the likelyhood of a geneticlaly susseptible person getting a autoimmune disorder?

A

Fermale hormones

A enviromental trigger such as infection

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12
Q

When would a test for Rheumatoid factor be high?

A

>70% positve in Rheumatoid arthritis

In other rheumatic disorders eg. Sarcoidosis and infections

Old age

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13
Q

Why is Rheumatoid factor not a accurate screen for Rheumatoid arthritis?

A

As age increases Rh factor also increases

>70years = 10-25%

Do not have to have RA for the test to be positive

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14
Q

Which gender is more susseptable to genetic diseases?

A

Female dominant

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15
Q

What are the clinical features of RA?

A

Often young-middle age females (20-50 years)

Pain and stiffness in joints

Gradual or sudden onset

Usually symmetrical, hands, feet, other joints

Often a family member has RA

Smoking increases risk of developing RA

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16
Q

What are the 3 S’s of inflamatory arthritis?

A

Stiffness

Early mornign joint stiffness lasting over 30 min

Swelling

Persistant swelling of one joint or more - especially hand joints

Squeezing

Squeezing of the joints is painful

17
Q

Regarding RA, what are the following?

  1. Gender prevalance
  2. incidence
  3. Prevalance
  4. Genetics
  5. Peak onset
A
  1. Female:Male = 3:1
  2. 30/100,000 pop/year
  3. 1% of the adult population
  4. Association with HLA-DR4 and HLA-DR1
  5. Between 20-50 years
18
Q

How would RA typically present in a patient?

A

Symmetrical arthropathy

Hands & feet > 80% cases

Early morning stiffness

Symptoms:

  • Systemic: fatigue, anorexia, weight loss
  • Low grade fever, anaemia
  • Articular- joint aching and stiffness
19
Q

Name 4 RA hand deformaties you may see on clinical examination

A

Early fusiform swelling

Ulnar deviation

Swan neck deformities

Boutonniere deformities

20
Q

In RA, what may be present on the joints of the hands?

A

Rheumatoid nodules

Packed ith fibroblasts

Normally seen alongside ulnar deviation

21
Q

Describe the pathogensis of RA

A

Inflammation of the synovium

Secondary changes then occurring in the cartilage

Circulating autoantibody – rheumatoid factor in 80% (seropositive arthritis).

This complexes to IgG to form immune complexes found in joint synovium, fluid and elsewhere.

Wayward immune response causes synovial inflammation

Recruitment of PMNs, macrophages and lymphocytes

Phagocytosis of immune complexes and release of lysosomal enzymes

Destruction of joint cartilage and recruitment of further inflammatory cells

Vasodilation causes redness and swelling

Hyperplasia of synovium and angiogenesis: vascular granulation tissue = pannus

Inflammatory cells in pannus destroy cartilage and bone and cause ankylosis (stiffening and fusion)

22
Q

What are the tests you would do for RA?

A

FBC : anaemia (anaemia of chronic disease)

ESR /CRP : moderately raised

Immunology:

•Rheumatoid factor (RF) : raised in ~70% of cases

(and in some healthy people)

•Anti-cyclic citrillunated peptides antibodies (Anti CCP): positive in ~60% patients with RA

23
Q

What would you see from a radiological investigations fo someone with RA?

A

Early disease:

X-rays usually normal

Detect synovitis on ultrasound or MRI

Late disease:

Soft tissue swelling

Juxta-articular osteopenia

Joint space narrowing

Erosion of bone

Loss of cartilage

Deformity

24
Q

Describe the analgesic treatment route for RA

A

ONLY TREATS THE SYMPTOMS/PAIN

Paracetamol

=>

Paracetamol and NSAIDS

=>

Weak opiod - Codiene

=>

Moderate opiod - tramadol

=>

Strong opiod - morphine

25
Q

Describe the combination treatment route for RA

A

Sulfasalazine + Methotrexate

Also use Analgesic therapys for pain

Corticosteriod therapy is used as a quick fix while the combination therapy takes effect

Biological therapies may also be used (best, but very expensive)

26
Q

Describe how corticosteroids work to treat RA

Give and example of a corticosteroid used to treat RA

A

Result in blanket immunosuppression

Administered orally or intra-articular

Prednisolone

Inhibition of trascription factors

=>

Reduced transcription of many cytokine genes e.g. ↓IL1, IL2 and TNF

=>

Reduced clonal proliferation of Th Cells

27
Q

Give examples of disease modifying drugs used to treat RA

A

Antiproliferative (cancer drugs)

Methotrexate (against folate activity)

Azathioprine (against purine synthesis)

Immunomodulator

Sulfasalazine

28
Q

What are the side effects of disease modifying drugs such as methotrexate?

A
  • Increased risk of infections
  • Teratogenic e.g. methotrexate (avoid if planning pregnancy)
  • GI-mouth ulcers, nausea, diarrhoea
  • Hair loss
29
Q

What are the pros and cons of using biological agents to treat RA?

Give examples of biological agents

A

Monocolonal antibody therapy (MAb)

Infliximab = Anti TNF

Rituximab = Anti CD20 on B cells

Specific to one single target

Very expensive (£6-9,000/patient/year)

NICE aproval needed

Must be administered by injection or infusion as they are protien drugs so will be digested on ingestion

30
Q

What is the general prognosis for someone diagnosed with RA?

Are there any potential complications?

A

In general, good providing there is early diagnosis, managment, disease control and treatment

<10% will become severly disabeld

Complications:

Periodic flare ups requiring drug therapy

Reduced immunity from immunosuppression

Complications of drug treatments

Year 1 Locomotion (18 decks)

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