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RA Flashcards

1
Q

What diseases are classified as Rheumatic Autoimmune?

A

Scleredema, SLE, RA, granulomatosis, Psoriatic disease, Sjorgens.

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2
Q

What clinical features are common to all autoimmune rheumatic diseases? -5=

A
  1. Malaise
  2. Fatigue
  3. Weight loss
  4. Myalgia
  5. Arthritis
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3
Q

How is RA defined according to ACR/EULAR 2010?

A

The presence of synovitis in at least one joint, the absence of an alternative diagnosis better explaining the symptoms and a total score of at least 6 (of 10) from:

  • 2-10 joints large = 1 point, 1-3 small joints = 2 points, 4-10 small joints = 3, >10 joints altogether = 5 points.
  • RF or ACPA, low positive = 2 points, high positive = 3 points.
  • at least a duration of 6 weeks = 1 point.
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4
Q

How is RA defined according to BSR?

A

Persistent joint inflammation affecting at least three joint areas, involvement of the metacarpophalangeal (MCP=knuckles?) or metatarsophalangeal joints or early morning stiffness of at least 30 mins duration.

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5
Q

What is the prevalence of RA?

A

3:1 in favour of females developing it.
0.81% of UK population. 1.16% of female population, 0.44% of male pop.
Increases with age until 75 then decreases.
Higher prevalence in colder areas of Europe.

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6
Q

What factors can predispose to RA development? [3]

A
  1. Genetic: HLA-DRB1
  2. Environmental triggers: viral, bacterial, smoking, periodontitis.
  3. Hormones or hormonal deficiency may promote development.
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7
Q

What genetic factor can predispose RA development?

A

HLA-DRB1

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8
Q

What environmental factors can predispose to RA development?

A

Viral infection
Bacterial infection
Smoking
Periodontitis

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9
Q

What shared epitope is carried by the vast majority of RA patients?

A

HLA-DRB1

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10
Q

What RA associated antibody is useful in diagnosing RA?

A

The Rheumatoid Factor (RF) which are antibodies to the Fc domain of IgG.

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11
Q

What are the other RA specific antibodies? [3]

A
  1. Anti-BiP
  2. Anti-Sa
  3. ACPA - anti-citrullinated protein antigen. (Fibrin etc)
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12
Q

What are the typical signs and symptoms of RA? [5]

A
  1. Disease onset is over weeks or months,
  2. Painful, stiff joints due to inflammatory synovitis
  3. Symmetrical swelling in small joints,
  4. Large joints only sometimes affected.
  5. Fatigue, flu-like symptoms, morning stiffness.
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13
Q

What skin manifestations of RA can occur?

A

Rheumatoid nodules, ulcers, vasculitis.

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14
Q

What CNS/PNS manifestations of RA can occur?

A

Cerebrovascular disease, mononeuritis multiplex as part of vasculitis, carpal tunnel syndrome.

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15
Q

What eye manifestations of RA are there?

A

Scleritis, episcleritis, sicca syndrome.

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16
Q

What assessment tools for RA exist? [6]

A
  1. Sharp score (radiology)
  2. Larsen index (radiology)
  3. ACR response criteria
  4. Eular
  5. DAS
  6. Health Assessment Questionnaire
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17
Q

What radiological evidence of early RA may be present? [3]

A
  1. soft tissue swelling, narrowing of joint space.
  2. loss of cartilage, erosions.
  3. Severe erosive damage to MTP joints of feet.
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18
Q

What is the DAS28 score?

A

Numerical scale of 0-10 which indicated current activity of RA disease.

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19
Q

What laboratory parameters would be evaluated when assessing a patient’s RA?

A

ESR, CRP, RF, FBC
Electrolytes, creatinine, hepatic enzyme levels.
Synovial fluid analysis.
Urinalysis.

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20
Q

What is the general prognosis of RA?

A

Variable, if untreated = generally poor.
Aggressive nature of RA can lead to a rapid decline in the patient’s QOL. Increased risk of comorbidity compared with general population.

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21
Q

What are the key indicators of a poor outcome in RA? [6]

A
  1. Genetics: HLA-DRB1 genotype is associated with more severe form of RA.
  2. Laboratory: High ESR or CRP level at outset. RF+ve, anti-CCP +ve.
  3. Clinical assessment: many active joints, poor functional scores (HAQs)
  4. Uneducated
  5. Poor
  6. Radiological lesions of early onset.
22
Q

What are the current management strategies for mild RA? (brief)

A

Analgesics as required.
NSAIDs +/- DMARDS.
Initial aggressive treatment with DMARDs and NSAIDS is the preferred treatment.

23
Q

What are the current management strategies for both moderate and severe RA? (brief)

A

Analgesics as required.
NSAIDS +/- DMARDS.
DMARDS +/- Biologics

24
Q

What current therapies are approved for symptomatic treatment of RA?

A

NSAIDS: such as ibuprofen, COX-2 inhibitors like celecoxib, normal analgesics like paracetamol.

25
Q

What type of drug is celecoxib?

A

COX-2 inhibitor, used in RA.

26
Q

Which drugs are used to prevent or impede joint damage and alleviate disease signs and symptoms?

A
  1. Glucocorticoids
  2. DMARDS: like methotrexate.
  3. Biologics: like anti-TNFalpha, B cell therapy.
27
Q

Why are glucocorticoids used in RA treatment?

A

To prevent or impede joint damage and alleviate disease signs and symptoms. They are a class of anti-inflammatory corticosteroid (prednisolone) in oral or local injection.

28
Q

What effect does IL-6 release by mast cells in synovial joint have? [2]

A
  1. Increased CRP levels.

2. T and B cell stimulation.

29
Q

What is the effect of IL-1 release by mast cells? [3]

A
  1. Increased recruitment of inflammatory cells.
  2. Increased release of metalloproteases.
  3. Increased osteoclast maturation and therefore bone destruction.
30
Q

Why does IL-1 release by mast cells lead to increased bone destruction?

A

IL-1 increases osteoclast maturation rate and therefore bone destruction.

31
Q

What causes mast cell activation?

A

Auto-antibody immune complex + Fc receptor.

32
Q

Why does Toclizumab cause a reduction in levels of CRP and B/T cell stimulation?

A

It blocks the IL-6 receptor and the IL-6 normally causes these effects.

33
Q

TNFalpha release by mast cells causes what? [5]

A
  1. Increased expression of endothelial adhesion molecules
  2. Increased T and B cell proliferation.
  3. IL-1 and IL-6 production
  4. Increased bone destruction.
  5. Increased systemic and synovial inflammation.
34
Q

Why does TNFalpha release by mast cells cause increased bone destruction?

A

TNFalpha release -> increased IL-1 and IL-6 production.
IL-1 increased osteoclast maturation rate.
Osteoclasts are responsible for bone destruction.

35
Q

Name 5 common anti-TNFalpha agents:

A
  1. Infliximab.
  2. Etanercept.
  3. Adalimumab.
  4. Certolizumab.
  5. Golimumab.
36
Q

What type of agent is infliximab?

A

Anti-TNFalpha. Murine + mouse.

37
Q

What is Anakinra?

A

An IL-1 inhibitor.

38
Q

How does Anakinra use lead to reduced bone destruction?

A

Anakinra is an IL-1 inhibitor. IL-1 causes:

  1. Increased recruitment of inflammatory cells.
  2. Increased release of metalloproteases.
  3. Increased osteoclast maturation and therefore bone destruction.
39
Q

What type of agent is certolizumab peg?

A

Anti-TNFalpha agent, murine + human + PEG.

40
Q

What are the difference between the anti-TNFalpha agents licensed for RA?

A 
Infliximab: murine and mouse.
Etanercept: human 
Adalimumab: human
Certolizumab: human + mouse + peg
Golimumab: human.
41
Q

What type of agent is Etanercept?

A

Anti-TNFalpha. Human.

42
Q

What are the fully human anti-TNFalpha agents?

A

Etanercept.
Adalimumab.
Golimumab.

Mouse + human: infliximab,
Mouse + human + peg: Certolizumab.

43
Q

What is Rituximab?

A

B cell depleting monoclonal anti-CD20 antibody.

44
Q

What type of agent is Adalimumab?

A

Anti-TNFalpha. Human

45
Q

How does Rituximab cause B cell depletion?

A

It is a monoclonal anti-CD20 antibody which leads to Fc receptor gamma mediated antibody dependent cytotoxicity, complement-mediated cell lysis, growth arrest, B cell depletion.

46
Q

How does Abatacept function in RA treatment?

A

Soluble receptor composed of CTLA-4 and Fc fragment of IgG. Blocks interaction of CD90 and CD86 with CD28 on T cells. May also have an CD28 independent action to inhibit lymphocyte activation and cause T cell death.

47
Q

Abatacept blocks the interaction between [BLANK] and [BLANK] with CD28 on T cells.

A

Soluble receptor composed of CTLA-4 and Fc fragment of IgG. Blocks interaction of CD90 and CD86 with CD28 on T cells. May also have an CD28 independent action to inhibit lymphocyte activation and cause T cell death.

48
Q

What is abatacept?

A

Soluble receptor composed of CTLA-4 and Fc fragment of IgG. Blocks interaction of CD90 and CD86 with CD28 on T cells. May also have an CD28 independent action to inhibit lymphocyte activation and cause T cell death.

49
Q

Which RA treatment blocks an interaction between CD90 and CD86 with CD28 on T cells.

A

Abatacept is a soluble receptor composed of CTLA-4 and Fc fragment of IgG. Blocks interaction of CD90 and CD86 with CD28 on T cells. May also have an CD28 independent action to inhibit lymphocyte activation and cause T cell death.

50
Q

What is ACPA?

A

Highly specific antibody for RA. Can be found up to 14 years before the onset of the first symptoms.
ACPA antibodies may present early in the disease and accurately predict the development of RA.

III (24 decks)

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