The science behind RA Flashcards
Definition
Chronic, bilateral, symmetrical, polyarticular, inflammation of te joints.
, typically the knuckles amd proximal interphalyngeal joints.
Panus?
Rheumatoid synovitis, so inflammation of the synovium etc -> characterised by inflammatory cell infiltration, synoviocyte proliferation and neoangiogenesis.
Occurs in which joint in the back?
Facet joints (synovial joints within the back. Remember will present as bilateral. Can differentiate from axial spondylitis through if the patient can hyperextend their neck back the way.
Do we get seronegative and sero positive? Which antibodies do we expect to see?
Yes. Anti-CCP and potentially also RF in sero-postitive. Seronegative is a clinical diagnosis, and the prognosis is generally much better.
Rf is classically igm ->
attaches to fc part of iggg
What is Sjogren’s syndrome?
Dyrness of salivary glands, mucous membranes and places that produce fluids. Its another automimmune condition and is therefore associated with other autoimmune conditions such as RA and SLE.
Genetic susceptibilities and polymorphins
HLADRB1 (part of HLA-DR4): also CTLA4, c-REL, PTPN22 are all genetic susceptibilities.
What environmental factors can affect ra
SMOKING!! Viruses inc: E-Coli, Mycoplasma, periodontal gingivalis and gut microbiome.
What is citrillation ad how does it impact ra?
It is a normal process but if it goes wrong it is when we can get anti CCP antibodies.
Hoow do we know tha b cells are involved in pathogenesis in ra?
Because of the response to retinxunab -> targets the CD20+ on B cells specifically. May not be of use in sero negative because they aren’t producing their anti ccp antibodies and so the b cell lymphocytes will probably be less active and involved in the pathogenesis.
What are plasma cells?
They are what b cells differentiate into when they start producing large amounts of antibodies.
*Imbalance too much inflammation and not enough control of it
(TRregs)
What are the systemic effects that can be seen in ra? What causes them?
SO very heavily influenced by IL-6 and TNF alpha.
Uncontrolled chronic inflammation.
Vascular and cardiac: More phatty deposits, and altered lipid metabolism.
Liver -> anaemia of chronic disease (IL-6 increases hepacidin -> dyregulation of iron)
Lung -> interstitial disease/fibrosis
Brain -> fatigue and secondary fibromyalgia
Muscles -> Sarcopaenia
Bone -> Osteoporosis
Secondary Sjogren’s syndrome
What produces the proteases and what does it cause?
Synovcytes, especially when they are in their crazy stage. Causes degeneration of the articular cartilage.
