RA, Osteoarthritis, Crystal Arthropathies Flashcards
Definition of rheumatoid arthritis Articular or extra-articular surfaces? Male:female ratio? Age group? Prevalence?
Defined as a symmetrical inflammatory arthritis affecting mainly the peripheral joints which if untreated can potentially lead to joint damage and irreversible deformities leading to loss of function and increased morbidity and mortality. It may start out in one joint, but is eventually symmetrical. It can affect any synovial joint.
Can affect both articular and extra-articular structures.
1:3
Can affect any age group.
Prevalence in the UK is about 1%.
Pathogenesis of RA
Mediated by what antigen?
Potential triggers?
HLA-DR4 mediated, although cause is unknown. Patients are genetically predisposed to the condition and an environmental trigger sets it off.
Potential triggers could include infections, stress, cigarette smoking -> cigarette smoking causes changes to proteins in the lung, body recognises these as foreign, and antibodies produced tend to affect joints.
What is the main structure involved in RA?
The synovium
In RA, synovium becomes inflamed, which produces more synovial fluid, and draws in inflammatory cells, which damage the joint.
Chronic synovium inflammation leads to bone erosion
Don’t forget - the first two joints C1/C2 in the spine are synovium lined. Other joints - hand joints, wrists, elbows, shoulders, TMJs, knees, hips, ankles, feet.
What is pannus?
What condition is it associated with?
Pannus – name given to vascular hypertrophy synovium – osteoclasts cause bone erosion; inflammatory cells also erodes bone + inhibit cartilage cells; synovial cells are stimulated again, causing swelling and inflammation. The increased vasculature makes it easier for inflammatory cells to invade the joint.
RA
Immunology of RA?
Antigen is presented to antigen presenting cell, which goes into overdrive and starts stimulating macrophages, which releases inflammatory cytokines; T cells also stimulate B cells which differentiate into immunoglobulins, all in all causing joint destruction and inflammation.
What does synovitis clinically manifest as?
Joint swelling and inflammation
What is early rheumatoid arthritis?
At what point is the therpeutic window of opportunity?
Defined as less than 2 years since symptom onset.
First 3 months-therapeutic window of opportunity.
What four things is diagnosis of rheumatoid arthritis based on?
Joint distribution - number and type (small or large) of joint affected
Serology - RF and ACPA
Symptom duration
Acute phase reactants - CRP and ESR
How is Hb affected in RA?
What about inflammatory markers?
Any inflammatory condition can cause anaemia (MCV is normal but Hb is low). It’s unusual to see synovitis with normal inflammatory markers.
What are some common symptoms in RA?
Pain in synovial joints
Prolonged morning stiffness
Involvement of small joints of hands and feet
Symmetric distribution
What is the squeeze test?
In RA - positive compression tests of metacarpophalangeal (MCP) and metatarsophalangeal (MTP) joints – if there is synovitis, there is pain
What are some clinical presentations of RA?
PIP, MCP, wrist, MTP synovitis -> swelling and pain Monoarthritis – around 30% of cases, remember to look out for RA in other joints Tenosynovitis Trigger finger Carpal tunnel syndrome Polymyalgia rheumatic Palindromic rheumatism Systemic symptoms Poor grip strength Extensor tenosynovitis
Which two antibodies can be positive in RA?
What is the sensitivity and specificity of each?
Rheumatoid factor (Rheumatoid IgM) - sensitivity 50-80%; specificity 70-80% Antibodies to cyclic citrullinated peptide (Anti-CCP antibodies); sensitivity-60-70%; specificity-90-99%
What other antibody might be associated with RA? When is this present? What does it correlate with? What SHx is it associated with? What outcome is it associated with? How does it change with treatment?
Anti-CCP
- Can be present for several years prior to articular symptoms
- Co-relates with disease activity
- Associated with current or previous smoking history
- More likely to be associated with erosive damage
- Anti-CCP ab patients remain positive despite treatment
Low sensitivity – absence does not exclude disease
X-ray in RA
Advantage?
What may it show?
Disadvantage?
Cheap and reproducible – think about getting baseline x-ray
Soft tissue swelling
Periarticular osteopaenia
Erosions
Disadvantage - absence of findings in early disease
What are some advantages of USS in RA?
Increased sensitivity for synovitis in early disease
Consistently superior to clinical examination
Can detect up to 7 times more MCP erosions than plain x-ray in early RA
Useful in making treatment changes
Advantages of MRI in RA?
Disadvantage?
Bone marrow oedema on MRI is associated with inflammatory joint disease and maybe a forerunner of erosion
Integrity of tendons can be assessed
Can distinguish synovitis from effusions
Can detect erosions earlier
Can be used to monitor disease activity
Limited by cost
Describe the RA treatment pyramid
It's an upside down pyramid - Immediate treatment is very important and theres lots of it - After remission is achieved, treatments are gradually withdrawn Initial treatment: - Aspirin/NSAIDs + steroid \+DMARD #1 \+DMARD #2 \+DMARD #3
Steroids in RA
- What do they do?
- What are they used in combination with?
- Administration?
Shown to improve RA symptoms and reduce radiological damage
Used in combination with DMARDs- not to be used as sole therapy
Can be given orally, IA or IM
DMARDs in RA
What are the common ones to use?
How should they be given
Methotrexate
Sulfasalazine
Hydroxychloroquine - DOES NOT PREVENT EROSIONS
Should be given as combination therapy
What is the initial drug of choice in RA?
Starting dose?
What supplement is required?
Initial drug of choice in RA
Start at 15 mg/week with rapid escalation
Folic acid 24 hours after MTX dose
