Clinical (Weeks 1+2) Flashcards
(183 cards)
What genes are associated with a susceptibility to RA?
HLA DR4
HLA DR1
What cells invade the synovium in RA?
Macrophages
Fibroblasts
Multinucleated giant cells
What is the basic process behind RA?
- Synovial expansion
- Invasion of bone
- Erodes bone and cartilage
Articular symptoms of RA?
Joint pain
Morning stiffness
Joint swelling
Extra-articular manifestations of RA
Respiratory: - Effusions - Fibrosis - Nodules Rheumatoid nodules on extensor surfaces Ocular involvement: - Keratoconjunctivitis - Episcleritis - Uveitis - Nodular scleritis Increased CVS morbidity and mortality
What hand joint is not affected by RA?
DIP
What pattern of joint involvement is seen in RA?
Symmetrical
How is RA defined by the EULAR/ACR Classification?
Synovitis in >/=1 joint Absence of better diagnosis Achievement of >/=6/10 of: - Number and site of affected joints (0-5) - Serological abnormality (0-3) - Increased CRP/ESR (0-1) - Symptom duration (0-1)
What is the best autoantibody to test for to aid in the diagnosis of RA?
Anti-CCP (Cycli citrullinated peptide) Antibody
Does a patient need to be Rheumatoid Factor positive (RhF) to have RA?
No
What chronic haematological change may be seen in RA?
Anaemia
What x-ray changes are seen in RA?
Osteopaenia:
- Loss of joint space
- Periarticular erosions
Soft tissue swelling
What late complications can be seen in RA?
Infection Cervical myelopahy secondary to: - Atlanto-axial/Subaxial subluxation ILD Peripheral neuropathy
What comorbidities is RA associated with?
Severe infections
CVS mortality
Lymphoma
What genetic factor is a poor prognostic factor in RA?
HLA DR4 positive
How soon must treatment be begun in RA to prevent irreversible damage?
Within 3 months
What are the principles of RA treatment?
DMARDs
Steroids to cover lag phase
Frequent reviews
Give examples of DMARDs and when they might be used?
1st line - Methotrexate
2nd line and in pregnancy - Sulphasalazine
Hydroxychloroquine
Leflunamide
What four approaches to biologic therapy can be used in RA and give examples of drugs in each class?
TNF-alpha inhibition: - Infliximab - Adalimumab - Etanercept B cell depletion: - Rituximab Disruption of T cell co-stimulation: - Abatecept Interleukin inhibition: - Anankira (IL-1) - Tocilizumab (IL-6) (Jak-2 inhibitors)
What is the pathogenesis of OA?
Loss of matrix (Collagen ii with chondrocytes embedded)
Cytokine release:
- IL-1
- TNF-alpha
- Metalloproteinases
- Prostaglandins from chondrocytes
Surface fibrosis and attempted repair -> Oestophytes
How are localised and generalised idiopathic OA defined
Localised: - Hands - Feet - Knee - Hip - Spine Generalised is >/= 3 sites involved
What are some secondary causes of OA?
Previous injury RA Genetic Acromegaly Crystal arthropathy Perthes SUFE
Risk factors of OA
Age Female Obesity Job Injury/Sports
When is pain typically present in OA?
During exercise