RHEUMATOID ARTHRITIS Flashcards

1
Q

What is RA?

A
  • an chronic autoimmune inflammatory disease of synovial joints
  • 1% of population
  • Can be subacute (20%) (fast) or insidious (70%) (gradual)
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2
Q

What are the causes of RA?

A

Causes still unknown, thought to have some genetic factors

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3
Q

Describe the pathophysiology of RA

A
  • Characterised by synovitis with thickening of the synovial lining and infiltration by inflammatory cells
  • auto-antibodies RF and anti-CCP–> cell mediated defective immune response–>Immunoglobulins and cytokines present in synovial fluid–>inflammation
  • synovium then proliferates and grows over articular cartilage–>tumour formation called pannus
  • pannus destroys the articular cartilage and subchondral bone, producing bony erosions
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4
Q

What are the risk factors for RA?

A
  • Gender: women 2-3x
  • Age: 40-60 most common
  • Family history
  • Genetic factors (HLA-DR4 and HLA-DRB1 confer susceptibility for RA)
  • Smoking
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5
Q

What are the signs of RA?

A
  • 4 signs of inflammation (rubor, calor, dolor, tumour)
  • Symmetrical and polyarthropathy of smaller joints
  • Loss of function
  • Deformity and damage
  • Extra-articular involvement (15-25% of cases)
  • Dorsal and lumbar spine are not involved
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6
Q

What are signs of deformity and damage in RA?

A
  • Swan neck (hyperextension at PIP, flexion at DIP)
  • Boutonniere (flexion at PIP, hyperextension at DIP)
  • Z thumb deformity
  • Ulnar deviation
  • Subluxation (partial dislocation) from weakening of joint capsules causing joint instability
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7
Q

What are the symptoms of RA?

A
  • Pain worse in the morning (lastings>30 min, may improve with activity)
  • Morning stiffness (can be several hours in bad cases)
  • General Fatigue and Malaise
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8
Q

What are the differential diagnoses of RA?

A
  • OA
  • SA
  • Symmetrical seronegative spondyloarthropathies
  • SA
  • SLE
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9
Q

What are the investigations for RA?

A
  • Bloods; Anaemia (normocytic, normochromic), thrombocytosis, High ESR / CRP
  • Test for autoantibodies; RF and anti-CCP, ANA
  • aspirate joint–>synovial fluid (exclude SA)
  • X-ray
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10
Q

What is seen on an X-ray for RA?

A
  • L - loss of joint space
  • E - erosions (focal)
  • S - soft tissue swelling
  • S - soft bones (osteopaenia - send for DEXA scan)
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11
Q

What are the extra-articular involvement on soft tissues in RA?

A
  • nodules (on fingers and pressure areas eg elbows)
    -bursitis
    tensynovitis
    -muscle wasting
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12
Q

What are the extra-articular involvement on eyes in RA?

A
  • Episcleritis
  • Scleritis
  • Necrotising scleritis
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13
Q

What are the extra-articular involvement on nervous system in RA?

A
  • Mild primarily sensory peripheral neuropathy
  • Legs>arms
  • Entrapment neuropathies- carpal tunnel
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14
Q

What are the extra-articular involvement on Haematological

system in RA?

A
  • Lymph nodes can be palpable
  • Spleen may be enlarged
  • Normochromic normocytic Anaemia
  • Haemolytic
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15
Q

What are the extra-articular involvement on lungs in RA?

A
  • Pleural effusion
  • Diffuse fibrosing alveolitis
  • Rheumatoid nodules
  • Caplan’s syndrome (rare, coal dust exposure)
  • Small airways disease
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16
Q

What are the extra-articular involvement on the heart in RA?

A
  • Pericardial rub
  • Pericarditis
  • Pericardial effusion

Increases risk of cardiovascular disease by 2-3x (same as type 2 diabetes)

17
Q

What are the extra-articular involvement on the kidneys in RA?

A

Amyloidosis

18
Q

What are the extra-articular involvement on the skin in RA?

A
  • Vasculitis

- ulceration

19
Q

What is the goal of treatment in RA?

A

No treatment cures, goal: remission of symptoms, return of full function and maintenance of remission with DMARDs.

20
Q

What is the non-pharmacological treatment for RA?

A
  • Rehabilitation (improve muscle power and maintenance of mobility to prevent flexion deformities.
  • Occupational therapy to find aids to reduce disability
  • Smoking cessation
  • Deal with depression / disability
21
Q

What is the pharmacological treatment for RA?

A
  • DMARDs (1st line treatment) eg Methotrexate, Sulfasalazine
  • Biological DMARDs- TNF-alpha inhibitors eg adalimumab
  • Steroids
  • NSAIDS
22
Q

Describe the course of DMARDs in RA

A
  • Start within 3 months of persisting symptoms
  • 6-12 weeks before benefit
  • Sulfasalazine: mild to moderate disease, and is drug of choice for many, especiall younger patients and women starting a family
  • Methotrexate: drug of choice for patients with more active disease. Contraindicated in pregnancy and should not be prescribed before planned conception
  • Leflunomide: blocks T cell proliferation. Has similar initial response rate to sulfasalazine but improvement continues and it is better sustained at 2 years. Used alone or in combination with methotrexate
  • Hydroxychloroquine, azathioprine and penicillamine used less frequently
23
Q

How do DMARDs work?

A
  • Inhibit inflammatory cytokines and thus slow development of joint erosion and irreversible damage
  • Reduces cardiovascular risk
24
Q

What are the S/E of methotrexate?

A
  • mouth ulcers
  • diarrhoea
  • liver fibrosis
  • pulmonary fibrosis
  • renal impairment
25
Q

What are the S/E of sulfasalazine?

A
  • Mouth Ulcers
  • Hepatitis
  • Male infertility (reversible)
26
Q

How do steroids work in RA?

A
  • suppress disease activity but dose required is often large, with considerable risk of long term toxicity
  • Start with oral corticosteroids
  • Local injections can improve pain but repeated are avoided because they might accelerate joint damage
  • IM methylprednisolone helps to control severe disease flares
27
Q

How do NSAIDS work in RA?

A
  • Effective in relieving joint pain and stiffness
  • Does not slow disease progression
  • Slow release preparations (eg slow-release diclofenac) can be taken at night to relieve symptoms the next day
  • Paracetamol with codeine (cocodamol) or without can be added for additional pain relief
28
Q

What are features which suggest poor prognosis in RA?

A

-insidious onset
-female sex
-increasing number of joints involved
-level of disability at onset
higher inflammatory and autoimmune markers
-signs of early erosive damage on imaging.