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Flashcards in MSK - Rheumatoid arthritis Deck (13)

contrast the outcomes of symptom- and disease-modifying RA treatments

key is early diagnosis and early intervention with disease-modifying anti-rheumatic drugs

DMARD: methotrexate is the gold standard and is first-line unless contraindicated

Biologic DMARD: indicated if inadequate response to DMARD

Symptomatic treatment (NSAID, corticosteroid): does not alter the course of RA


Describe a mechanical joint pain

•Chronic pain (months to years)
•Slowly worsening
•Worse with movement
•Improved by rest
•Not much swelling
•Little stiffness (10 – 15 minutes only)


Describe an inflammatory joint pain

•Acute or subacute pain
•May worsen quickly
•Better after movement
•Worse after rest
•Swelling often noticeable and may be prominent
•Stiffness may be prolonged (hours) and worse in the morning

Common Px of RA:
• Morning stiffness >1 h, improves
with use
• Symmetric joint involvement
• Initially involves small joints of hands
and feet
• Constitutional symptoms


Ix of a suspected RA (think of your 4 DDx)

- Rheumatoid factor
- Anti-citrullinated protein antibody (ACPA)
- Antinuclear antibody
- Parvovirus B19 antibody

To DDx:
–Rheumatoid arthritis
–Systemic lupus erythematosus
–Psoriatic arthritis
–Parvovirus associated arthritis


What are treatment goals in RA?

–Reduction of joint inflammation
–Prevention of joint damage
–Prevention of long-term RA-associated complications
–Avoid drug complications
–Maintenance of quality of life- decrease pain and stiffness


What (4) treatment strategies are there for RA?

–Pharmacological therapy
•non-steroidal anti-inflammatory drugs
•disease modifying anti-rheumatic drugs (DMARDs)

–Self-management - exercise, diet, joint protection, therapeutic compliance, education, personal empowerment

–Allied health intervention - physiotherapy, occupational therapy, orthotists etc



Describe NSAIDs use in RA
- mechanism
- Cx
- efficacy

–Mechanism - decrease prostaglandin production by cyclo-oxygenase inhibition. (2 iso-enzymes, COX-1 and 2)

–Complications - Peptic ulcers, mouth ulcers, enteropathy, rashes, hepatotoxicity, renal toxicity

–Efficacy - good short and long term efficacy in inflammatory arthritis


List (4) DMARDS (disease modifying anti-rheumatic drugs) & (4) biologic DMARDS

Disease modifying anti-rheumatic drugs (DMARDs)

Biologic DMARDs
–TNF inhibitors – etanercept, adalimumab, infliximab, golimumab, certolizumab
–B cell inhibitor – rituximab
–Cell adhesion inhibitor – abatacept
–Il-6 inhibitor - tocilizumab


Describe Corticosteroids use in RA (oral & intra-articular)
- Cx
- efficacy

Oral prednisolone
- efficacious
- but causes hypertension, weight gain, skin changes, hyperglycaemia, osteoporosis

Intra-articular steroids
- Efficacious in accessible joints
- few side effects if used intermittently


How do you measure disease ACTIVITY of RA to determine response to treatment?

–Patient and physician global assessment (often using a visual analogue scale)
–Swollen and tender joint count (on examination)
–Measures of inflammation (ESR or CRP)


How do you measure disease DAMAGE of RA to determine response to treatment?

•Bone and cartilage damage occurs more slowly than soft tissue swelling.
•MRI more sensitive than plain Xrays for detecting synovitis, cartilage damage, bone oedema and bone erosions.
•Xrays usually not required in early management


What is RA an independent risk factor for?

atherosclerosis and CV disease

RA is associated with increased overall mortality/morbidity from all causes: CV disease, neoplasm (especially lymphoma), infection.


What (6) types of joint deformities of digits can you get in RA?

- Boutonniere deformity
- Swan neck deformity
- Z deformity of the thumb

- Claw toe
- Hammer toe
- Mallet toe

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