Rheumatoid arthritis Flashcards
Describe
Chronic, Autoimmune type III Hypersensitivity reaction
Principally affects the joints (synovial especially) but may also affect other organs
Symmetrical deformation of joints
Pain is worse in the morning
Clinical presentation
Insidious onset of pain in the Distal Small joints Morning stiffness (>30 mins) / Pain is worse in mornings Hand Deformities e.g. Ulnar deviation, swan neck and boutonniere Symmetrical deformation of joints
Pathophysiology
Infiltration of the synovium by inflammatory cells
- > Angiogenic cytokines
- > Formation of new synovial blood vessels
- > Synovium proliferates and grows out over the surface of cartilage producing a pannus
- > Pannus damages the cartilage and subchondral bone below, by blocking its normal route for nutrition and by effects of cytokines on the chondrocytes
- > Bony erosions
Aetiology
HLA DR4 and HLA DR1 confer susceptibility
Triggering antigen not known, but thought to be a type III hypersensitivity reaction
Epidemiology
1% of population will experience
More common in women
Peak incidence in 40s
Diagnostic tests
Anti-CCP (marker of disease but not pathogenic itself)
Rheumatoid factor - also AntiNuclear antibody
X-ray
Normochromic normocytic anaemia on bloods
Describe X-ray of Rheumatoid arthritis
(Peri-articular erosions) Juxta-articular osteopenia Soft tissue swelling Joint deformity Loss of joint space (Also osteopenia - soft bones)
Treatment
DMARDs e.g. Methotrexate (oral)
NSAIDs and COX inhibitors (relieve joint pain and stiffness) and paracetamol +/-opioid (for pain management)
TNF- alpha inhibitor (slows/halts erosion formation)
Physiotherapy
Interarticular corticosteroid injection (semicrystalline steroid)
Complications of rheumatoid arthritis
Carpal tunnel syndrome Cervical myopathy Pericarditis Tendon rupture Sjogren's syndrome Social impact and depression
How can you tell the difference between rheumatoid and osteo-arthritis
OA is defined as joint stiffness caused by loss of cartilage between joints due to wear and tear, while RA stems from an autoimmune attack on joints.
RA - get more generalised symptoms (not present in OA); frequent fatigue; morning stiffness >1 hour; relatively rapid (wks to months)
OA - morning stiffness <1 hour; slow (years); more later in life
Examples of TNF-alpha inhibitor
Infliximab (IV monoclonal antibody)
Adalimumab (SC monoclonal antibody)
Examples of DMARDs (oral)
Sulfasalazine (for mild/moderate disease) used in young and women
Methotrexate (gold standard for more active disease, CI in pregnancy)
What does DMARD stand for
Disease-modifying antirheumatic drugs
Side effects of Methotrexate DMARD
Nausea, mouth ulcers, diarrhoea, abnormal LFTs, neutropenia, thrombocytopenia, renal impairment
RA (inflammatory) vs OA (degenerative)
Age at which condition starts
RA = any time in life OA = usually begins later in life
RA (inflammatory) vs OA (degenerative)
Speed of onset
RA = relatively rapid, over wks to months OA = slow, over years
RA (inflammatory) vs OA (degenerative)
Joint symptoms
RA = joints are painful, swollen and stiff OA = joints ache and may be tender but have little or no swelling
RA (inflammatory) vs OA (degenerative)
Pattern of joints affected
RA = often affects small and large joints on both sides of the body (symmetrical), such as both hands, both wrists or elbows or balls of both feet OA = symptoms usually begin on one side of the body and may spread to the other side; symptoms begin gradually and are often limited to one set of joints - usually finger joints closest to the fingernails or the thumbs, large weight-bearing joints (hips and knees) or the spine
RA (inflammatory) vs OA (degenerative)
duration of morning stiffness
RA = morning stiffness lasts >30 mins OA = morning stiffness lasts <30 mins, stiffness returns at the end of the day or after periods of activity
RA (inflammatory) vs OA (degenerative)
presence of symptoms affecting the whole body (systemic)
RA = frequent fatigue and a general feeling of being ill are present OA = whole-body symptoms are NOT present
What is anti-ccp
Anti-Cyclic Citrullinated Peptide
Give examples of hand deformities seen in rheumatoid arthritis
Ulnar deviation
Swan neck/Z thumb
Boutonniere deformity
Pathophysiology again but more detail
- RA is primarily a synovial disease and synovitis (inflammation of the synovial lining) occurs when chemoattractants produced in the joint, recruit circulating inflammatory cells
- Over-production of TNF-alpha leads to synovitis and joint destruction, driven by the interaction of macrophages, T and B lymphocytes
- Synovium becomes greatly thickened and becomes infiltrated by inflammatory cells
- Angiogenic cytokines induce generation of new synovial blood vessels and activates endothelial cells to produce adhesion molecules that FORCE Leucocytes into the synovium, where they can trigger inflammation
- The synovium proliferates and grows out over the surface of the cartilage (past the joint margins), producing a tumour-like mass called ‘pannus’
- This pannus of inflamed synovium DAMAGES the underlying cartilage by blocking its normal route for nutrition and by direct effects of cytokines on the chondrocytes
- The cartilage becomes thin and the underlying bone exposed
- The pannus DESTROYS the articular cartilage and subchondral bone resulting in bony erosions
What is the name of the tumour-like mass formed by the proliferation of the (inflamed) synovium over the surface of the cartilage
Pannus
