Rheumatoid arthritis Flashcards
What is RA?
autoimmune, systemic, inflammatory disease
chronic, persistant synovial inflammation = destroys articular cartilage and bone = decline joint function
what are the common symptoms of RA?
- symmetrical polyarthritis
- pain and swelling
- affecting small joints of the hands and feet
- morning stiffness
- improves with activity (ideally)
- debilitating fatigue
what are the clinical symptoms of RA?
- increase level of acute phase reactants (CRP)
- increase level of erythrocyte sedimentation rate (ESR)
- autoantibodies for RA (RF) and anti-citrillinated protein autoantibodies (ACPA)
what joints does RA affect?
MCP joints
PIP joints
MTP joints
professing to the wrists, ankles, knees
what is the pathology of OA?
thin cartilage
bones rub together
what is the pathology of RA?
swollen inflamed synovial membrane
bone erosion
why is RA scary (arghhh)?
decreased life expectancy due to co morbidities
what co-morbidities are associated with RA?
-atheroscloersis and heart disease
-vasculitis
-lung inflammation and resultant scarring
-infection risk due to immunosuppressant treatment (ANTI- TNF-a, corticosteroids)
-high risk of lung cancer and lymphoma
what lifestyle advice would you advise for RA pt’s?
stop smoking
control weight
blood pressure
cholesterol
early and effective treatment to reduce symptoms to reduce systemic inflammation
what is the criteria to diagnose RA?
score >6/10
what are the risk factors of RA?
-age
-female
-genetic predisposition - hereditary/HLA-DBR-1 gene variant
environmental factors
-smoking
-dust/silica exposure
-microbes
what is the HLA-DBR-1 gene variant responsible for?
it does not result in RA, but increases the risk factors majorly for RA
what are RF’s?
autoantibodies that recognise Fc portion of IgG for RA known as rheumatoid factors
what tool is used to diagnose RA?
The anticyclic citrullinated peptide (anti-CCP) assay broadly detects antibodies against citrullinated proteins (ACPAs) and has high specificity and excellent sensitivity in RA
known as RF’s
what risk factors increase APCA formation?
-periodontal tissue bacteria
-lung smoke/air pollutant
-intestinal bacteria
how is APCA produced?
T cell stimulates B cell to produce autoantibodies
why is early detection important
as early treatment showed lower levels of disease progression
what cells migrate into the joint from the blood in RA?
- neutrophils
- early in inflammation produces IL-17 cytokines - dendritic cells
-activates T cells w antigen produces IL-12, IL-23 turn T cell on IL-10 T cell off - effector cells
-help b cells make antibodies - b cells
-make antibodies - regulatory cells
-make IL-10 to turn off immune response
what cells are in the joint?
1.Chondrocytes
-Make metalloproteinase enzymes to degrade cartilage
2. Fibroblast-like synovial cells
-Make metalloproteinase enzymes and invade and degrade cartilage and bone. Secrete cytokines e.g. IL6 to attract and retain leukocytes in the joint
3. Macrophage
-Make lots of cytokines to activate osteoclast and immune cells
4. Osteoclast
-Make enzymes and degrade bone
5. Mast cells
-Make vasoactive factors that attract immune cells to the joint
6. Adipocytes
-Make anti-inflammatory adipokines (e.g. leptin)
what are the two aims of RA treatment?
- slow disease progression
- control symptoms
what is DAS28 score?
clinical assessment to score disease activity
what is measured in DAS28?
what does a high/low/remission score in RA?
what are disease modifying anti-rheumatic drugs (DMARD)
