Rheumatoid Arthritis Flashcards
(27 cards)
What are rheumatoid factors?
An IgM antibody that works against IgG antibodies
Line vasculature (e.g. spleen) and attach to passing antibodies
Seen in old age, chronic infections and rheumatoid arthritis
Why should rheumatoid factors not be used as a routine screening tool?
Rheumatoid factors seen in population anyway particularly with ageing (seen in 10-25% of people over 70)
Should only be used if history indicates rheumatoid arthritis (joint pain alone does not indicate rheumatoid!)
What clinical features in a history could indicate rheumatoid arthritis?
Often young to middle age females (20-50 years)
Pain and stiffness in joints
Gradual or sudden onset
Usually bilateral (hands, feet and other joints)
Genetic link (family member with RA)
Smoking increases risk
What is the ‘S’ factor?
Indicators of RA:
Stiffness (>30 mins in morning)
Swelling
Squeeze (pain or tenderness when squeezing joint)
Which genes are linked to rheumatoid arthritis?
HLA-DR4
HLA-DR1
What is the classic distribution of rheumatoid arthritis?
Hands/ fingers
Ankles/ toes
Knees
What are the symptoms of rheumatoid arthritis?
Joint aching and stiffness (esp. hands and feet)
Early morning stiffness (improves within couple of hours normally)
Systemic symptoms e.g. fatigue, weight loss, anorexia, anaemia, low-grade fever
What hand deformities can present in rheumatoid arthritis?
Fusiform swelling
Ulna deviation
Swan neck deformities
Boutonniere deformities
What extra-articular manifestations can appear in rheumatoid arthritis?
Cardiac (e.g. pericarditis, valve problems, atherosclerosis, ischaemic heart disease)
Pulmonary (e.g. pleural effusions, pulmonary fibrosis)
Blood (e.g. anaemia)
Bones (e.g. osteoporosis)
Skin (e.g. leg ulcers, vasculitis)
Neurological (e.g. nerve compression)
Eyes (e.g. scleritis, xerophthalmia)
What can be done in rheumatoid arthritis to minimise the chance of developing ischaemic heart disease?
Address risk factors e.g. smoking, high cholesterol, obesity Treat hypertension (if present)
What is the pathogenesis of rheumatoid arthritis?
- T-cell mediated immune response
- Inflammatory response
- Release of cytokines (TNF, IL-1)
- Pannus formation (caused by angiogenesis of synovium and synovial proliferation)
- Release of enzymes (e.g. protease) and PGs resulting in cartilage breakdown
- Synovial joint destruction
What blood test results would we expect to see in a patient with rheumatoid arthritis?
FBC: anaemic ESR/ CRP: moderately raised Rheumatoid factor: raised Anti CCP: positive ALP: raised Albumin: decreased
Why can people with rheumatoid arthritis develop anaemia?
Active disease (anaemia of chronic disease)
Blood loss
Drugs can suppress bone marrow
Felty’s syndrome (rare complication of rheumatoid arthritis causing splenomegaly)
What would we expect to see in imaging of patients with rheumatoid arthritis?
LESS:
Loss of joint space
Erosions (“punched out” areas of bone)
Soft tissue swelling
Sublaxation (causing ulna deviation and swan neck deformities, can also be seen at atlantoaxial joint in cervical spine)
What analgesia should be used to manage pain in rheumatoid arthritis?
1st line: Paracetamol 2nd line: NSAIDs + paracetamol 3rd line: Weak opioid (e.g. codeine) 4th line: Moderate opioid (e.g. tramadol) 5th line: Strong opioid (e.g. morphine)
What is the current strategy for treating RA?
1st line: disease-modifying anti-rheumatic drugs [Methotrexate + Sulfasalazine in combination]
+ NSAIDS
+ Corticosteroids (e.g. prednisolone) short term
2nd line: Biologic therapies
How do corticosteroids work to treat RA?
Inhibition of transcription factors leading to reduced transcription of cytokine genes (e.g. interleukins and TNF) which leads to reduced clonal proliferation of T helper cells
How does Methotrexate work to treat RA?
Inhibits DNA synthesis by inhibiting folate pathway
Reduces lymphocyte proliferation
What anti-proliferative drugs are used in RA managament?
Methotrexate
Azathioprine
What immunomodulators are used in RA management?
Sulfasalazine
How does Azathioprine work to treat RA?
Inhibits DNA synthesis by inhibiting purine pathway
Reduces lymphocyte proliferation
How does Sulfasalazine work to treat RA?
Mechanism unclear
? Possible COX inhibition
What are the potential side effects of anti-proliferative drugs?
Increased risk of infection
Teratogenic (should avoid in pregnancy!)
GI symptoms (e.g. mouth ulcers, nausea, diarrhoea)
Hair loss
What biologic agents can be used in RA management?
Monoclonal antibody therapy (MAb):
Anti TNFa (infliximab)
Anti CD20 on B cells (rituximab)
