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Rheumatology > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is the aetiology of RA?

A

RA is a chronic inflammatory disease of unknown aetiology

It is likely to involve an unknown stimulus which activates the innate immune system triggering cytokines, complements, NK cells and nuts. Dendritic cells present Ag to T cells which proliferate and produce inflammatory cytokines (TNF alpha + others). This stimulates macrophages, fibroblasts to release TNF -alpha, IL-6, IL-15 and 18 which leads to activation of proteases, neutrophils, B cells. Osteoclast are activated by macrophages via RANK-L.

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2
Q

What is the pattern of joint involvement?

A

symmetric, peripheral polyarthritis

  • earliest joints affected are the small joints of the hands and feet
  • once RA is established the wrists, MCPs and PIP joints are commonly affected (not DIPs)
  • may be monoarticular, oligoarticular (4+) or polyarticular (>5)
  • inflammation of joints, tendons and bursa
  • flexor tendon synovitis is a hallmark of RA -> decreased ROM, reduced grip strength, trigger fingers
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3
Q

What are the extra-articular features of RA?

A
  • subcutaneous nodules, secondary Sjogrens syndrome (10%), and anaemia are the most common
  • also fatigue, lung involvement, pericarditis, peripheral neuropathy, vasculitis, haematological abnormalities
  • more likely to develop if Hx of smoking, early onset of significant disability, positive RhF
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4
Q

What are the characteristic symptoms of RA?

A

Early morning joint stiffness lasting longer than 1 hour which improves with activity.

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5
Q

What are some of the more advanced features of RA

A

progressive destruction of the joints, soft tissues and tendons lead to deformities

  • ulnar deviation from subluxation at the MCPJs
  • swan neck deformities - hyperextension of PIPJ with flexion of DIPJ
  • boutonniere deformities - flexion of PIPJ with hyperextension of DIPJ
  • Z line deformity - subluxation of 1st MCPJ with hyperextension of 1st IPJ
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6
Q

What other joints can be involved?

A

knees and shoulders in advanced disease
atlantoaxial involvement of the C-spine
- can result in compressive myelopathy and neurological dysfunction

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7
Q

What is the sensitivity and specificity of RF and anti-CCP?

A

RF occurs in 70-80% patients with RA but also 5-10% of the general population
20-30% of patients with SLE have positive RF
Anti-CCP has specificity of 95-98% and similar sensitivity as RF

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8
Q

Which tests are positive in RA?

A

RF and anti-CCP - but both tests can be negative in 50% of RA
ESR and CRP are likely to be raised
ANA in 1/3 patients (DDx SLE)

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9
Q

What FBC changes might you see in RA?

A

anaemia of chronic disease, thrombocytosis

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10
Q

What are the diagnostic criteria for RA

A

2010 guideline is a scoring system where you get points for number of joints, serology, inflammatory markers and duration of symptoms
- you must score 6+ to achieve diagnosis

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11
Q

What are some Ddx?

A 
Seronegative RA (negative RF and anti-CCP
Recent onset RA (
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12
Q

What are the treatment options in RA

A 
NSAIDs
Steroids
Antimalarials - Hydroxychloroquine
DMARDS - MTX, Leflunomide, Salazopyrin
Biologics
Surgery if requires
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13
Q

What is co-stimulation of the T-cell

A

Antigen specific binding of T-cell to APC through MHC (major histo-compatibility complex) AND costimulation through the CD28-CD80/86 pathway is required to activate the T-cell (otherwise it dies or doesn’t do anything)

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14
Q

What pathway activates osteoclastogenesis in RA

A

Driven by macrophages through interaction of RANK and RANK-L (ligand)

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15
Q

What are the main cytokines involved in RA

A

TNF alpha
IL 1
IL 6
IL 17

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16
Q

What are the t-cell CD4 subsets involved in RA

A

TH1

TH17

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17
Q

What is pannus?

A

Pannus is abnormal inflammatory tissue found between cartilage and bone, cells in pannus produce protienases which destroy cartilages

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18
Q

What is VEGF and why important in RA

A

Vascular endothelial growth factor - enables pannus to obtain its on blood supply through angiogenesis

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19
Q

Why do you get anaemia of chronic disease?

A

IL-6 causes production of hepcidin (an acute phase protein) which inhibits iron release from macrophages and reduces iron uptake in duodenum = anaemia

20
Q

What is the genetic contribution to RA?

A

10-25%

21
Q

What are some genetic mutations implicated in RA

A

HLADRB1
STAT 4
PADI 4
PTPN22

22
Q

Prevalence of RA

A

1%

23
Q

Sex distribution of RA

A

2-3 F: 1M

24
Q

What are the four categories in the classification criteria for diagnosis of RA?

A

Joint involvement (number and size) - with synovitis
Serology (RF and anti-ccp)
Acute phase reactants (ESR, CRP)
Duration of symptoms (either less then or greater then 6 weeks)
Score of 6 or greater indicates likely RA

25
Q

What are some non-pharmacological therapies for RA

A 
PT
OT
Nutrition
Reduce cardiovascular risk
Immunisations
Smoking cessation
26
Q

What tests should be performed before commencing treatment of RA

A 
Hepatitis B and C
Screen for latent Tb
- if present must be treated with Isoniazid for one month prior to initiating treatment and continued for 6 months
Ophthalmologist evaluation if using hydroxychloroquine
Baseline blood with LFTs
Pregnancy test
Lipid and glucose testing
CXR
27
Q

What are the four mechanisms by which biological DMARDs work?

A

TNF alpha inhibition
B-cell depletion
Co-stimulation blockade
Inhibition of IL 1 and IL 6

28
Q

What is an IL-1 inhibitor used in RA

A

Anakinra

29
Q

What is an IL-6 inhibitor used in RA

A

Tocilizumab

30
Q

What is a t-cell co-stimulation inhibitor?

A

Abatacept

31
Q

What is the main b-cell depleting agent used in RA

A

Rituximab

32
Q

What are 4 examples of TNF alpha blockers used in RA

A 
Infliximab
Adalimumab
Golimumab
Certolizumab
Ertanercept
33
Q

What should you screen before staring hydroxychloroquine?

A

Ophthalmological exam then every 6-12 months on treatment

34
Q

What is a rare neurological side effect of leflunomide

A

Peripheral neuropathy

35
Q

What 4 features most accurately predict a diagnosis of RA?

A
  1. arthritis of the hands
  2. positive RF or anti-CCP
  3. Morning stiffness for > 1 hour
  4. MRI bone oedema
36
Q

Name 4 features that predict a poor outcome in RA (there are more than 4)

A
  • sustained elevation of CRP
  • Extra-articular features
  • HAQ > 1 at 1 year
  • multiple joints involved (>12)
  • MRI bone oedema
  • Joints with power doppler US signal - these joints tend to erode
  • High titres of RF and/or anti-CCP - erosions are more common in seropositive disease
  • Low SES/education
  • Female
  • Advanced age at onset
37
Q

What is the DAS28?

A

a scoring system of disease activity which includes:

  • number of tender joints (28 joints)
  • number of swollen joints (28)
  • ESR
  • patient rates the global activity of arthritis in the past week out of 100 - 0 = no symptoms, 100 = very severe

the score is calculated using a computer scoring system
DAS28 5.1 = high
DAS28

38
Q

What pharmacotherapy would you use to manage RA with low disease activity?

A

DMARD monotherapy
- usually MTX

  • if features of poor prognosis present - combination DMARD (double or triple therapy)
  • MTX + Leflunomide or Salazopyrin
39
Q

What pharmacotherapy would you use to manage RA with high disease activity?

A

DMARD mono therapy or HCQ + MTX

  • if features of poor prognosis present
  • combination DMARD therapy (double or triple therapy)
    or anti-TNF + MTX

in NZ have to have trialled combination DMARD before qualifying for anti-TNF

40
Q

What 3 anti-TNF drugs are used in RA?

A

Adalimumab (Humira = humanised mAB, given SC)
Infliximab (chimeric, given IV)
Etancercept (TNFreceptor:Fc fusion protein, given SC)

41
Q

What are the main side effects of TNF alpha inhibitors

A
  1. infection risk: Hazard ratio = 1.2 - 1.5 for serious infection
  2. susceptibility to intracellular pathogens
    - reactivation of latent TB
  3. reactivation of HepB
    (TNFaplha suppresses HBV replication)
    - monitor serology 3 monthly and consider anti-viral prophylaxis
  4. Risk of cancer is controversial - possible increase risk of lymphomas, although there is a baseline increased risk with RA alone
    - consider using rituximab instead of TNF-inhibitors if Hx of malignancy
  5. May worsen CHF - avoid

rare: exacerbation of previous quiescent MS, optic neuritis, ILD

42
Q

What is the ACR-70?

A

A standard measure of the number of people who have 70% or greater improvement according to 7 clinical and laboratory measures of disease activity.

43
Q

What are the benefits of TNF inhibitors?

A
  • reduce erosions
  • decrease disability as assessed using HAQ
  • improve QOL
44
Q

Are TNF inhibitors the most effective drug for RA when used alone?

A

No - trials have shown that TNF inhibitors in combination with MTX are more effective than mono therapy with either MTX or TNF inhibitors.

There has only been one head to head trial of MTX + anti-TNF vs combination DMARD which showed only a modest benefit

45
Q

What is the main role of steroids in the management of RA?

A

Disease flares

46
Q

What vaccinations should be considered?

A 
Inactivated vaccines:
Pneumovax
Flux
Hep B
Diphtheria/Pertussis/Tetanus/Polio

Live vaccines:
Zoster
- before starting immunosuppression

47
Q

What treatment should be used for RA in pregnancy?

A

May often have lower treatment requirements

  • NSAIDs - stop 3rd trimester (closure of ductus)
  • DMARDS - Sulphasalazine, hydroxychloroquine and prednisone are probably safe
  • anti-TNFs: stop before 30 weeks and do not vaccinate baby with live vaccines
  • Rituximab - stope at 12 weeks before delivery (B cell depletion in neonate)

Rheumatology (11 decks)

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