Rheumatoid Arthritis Flashcards
what is RA
symmetrical inflammatory arthritis affecting mainly the peripheral joints
if untreated what can RA lead to
joint damage, irreverisble deformities, loss of function, increased morbidity and mortality
who is more likely to get it men or women
women (x3)
what age group can be affected by RA
any
what part of spine can be affected
just C1 and C2
what gene mediates RA
HLA-DR4
what are the potential triggers for RA
smoking, infections, stress
what do the severity and course of RA depend on
genetic factors and presence of auto antibodies
what is the link to smoking
smoking cause proteins in the lungs to become citrullinated (irreversible) and antobodies are created against these which also target the joints
what is the main structure involved in RA and how is it affected
synovium- gets thickened and inflammed
what is the synovium
lines the inside of joint capsules and tendon sheaths
what joints are synovial
C1,C2, hand, wrists, elbows, shoulders, TMJs, knees, ankles, feet, hips
what is a pannus and how is it formed in RA
an abnormal layer of fibrovascular tissue or granulation tissue
Inflammation and exuberant proliferation of the synovium leads to formation of pannus and destruction of cartilage, bone, tendons, ligaments, and blood vessels. Pannus= the hypertrophied (enlarged) synovium
how is the inflammatory cascade perpetuated
inflamed synovium caused increased blood flow- more antibodies and inflammatory cells
how does bone erosion occur in RA
as osteoclasts activated by proinflammatory cytokines
cartilage cells are prevented from being regenerated
describe the immune pathogenesis of RA
antigen (unknown) presented to niave T cells which is activated and stimulates B cells to produce rheumatoid factor and IL-6 and macrophages to produces IL-1 and 6 and TNF alpha
net result is osteoclast stimulation, hypervascular pannus and destruction of cartilage and joint
what is the theraputic window for rheumatoid arthritis
when it is in early stages (first three months)
what defines early RA
less than two years since symptom onset
what is tendonsynovium
the synovium surrounding a tendon, can be affected by RA
the involvement of larger or smaller joints produces a higher ECR/EULAR score
smaller joints
what are the symptoms of RA
will be fit and well then joints will start to be sore
early morning stiffness lasting 30-hour or even until lunchtime
swelling of the joints that is symmetrical and tender
involvement of small joints of hands and feet
positive compression tests of metacarpophalangeal (MCP) and metatarsalangeal (MTP) joints
why do you get early morning stiffness
as synovial fluid gets thicker overnight due to lack of movement
what diagnostic tests can be done
mostly history and clinical exam
blood tests- anaemia of chronic disease, raised platelets
inflammatory markers (CRP, ESR, plasma viscosity)
autoantibodies (seen in 70% of cases)
imaging (x rays of hands, feet and chest as a baseline)
systemic exam- listen for involvement of the lungs, test reflexes and sensations
what does RA in the feet feel like
walking on pebbles
what is monoarthritis
rare- when one joint in inflamed
what is tenosynovitis
inflammation of tendons (rare)
what is trigger finger
clinical presentation of RA, when finger gets stuck in flexed position then extends with a click
how many patients with RA have bilateral carpal tunnel syndrome
15%
what is polymyalgia pheumatica
muscle pain, stiffness and inflammation in the muscles surrounding the neck, shoulder and hips
what is palindromic rheumatism
variant of RA that comes and goes- usually progresses to complete RA
how is grip affected in RA patients
reduced- many unable to make a fist
what is extensor tenosynovitis
swelling in the extensor tendons
tendons flare and tear
what is synovitis
inflammation of the synovial membrane
what happens to the muscles in synovitis
waste due to the inflammation
what autoantibodies are associated with RA
rheumatoid factor (rheumatoid IgM)
antibodies to cyclic citrullinated peptide (anti-ccp antibodies)
anti-ccp antibodes have higher sensitivity and specificity
describe the link between RA and anti-ccp antibodies and what they are associated with
can be present for several years prior to articular symptoms
associated with erosive damage
remain positive despite treatment
associated with smoking
what does the low sensitivity of antibodies mean
absence does not exclude the disease
what imaging can be done for RA
x rays
ultrasound
MRI scans
what do xrays show
soft tissue swelling
periartiuclar osteopaenia
erosions
OR nothing in early stages
what do ultrasound scans show
increased sensitivity for synovitis in early disease
erosions
increased blood flow to inflamed synovium
what do MRI scans show
bone marrow oedema (associated with inflammatory joint disease and possible precursor to erosions)
integrity of tendons
can distinguish synovitis from effusions
detects erosions earlier
can monitor disease activity
(most sensitive but limited by cost)
what and how many joints are affected by RA
28 in total 10 PIPs 10 MCPs 2 wrists 2 elbow 2 shoulders
what are the DAS288 scoring parameters
> 5.1 active disease
- 2-5.1 moderate
- 6-3.2 low disease activity
<2.6 remission
what is the treatment for RA
disease modifying anti rheumatic drugs
NSAIDs and steriods only s adjuncts (steroids bridge until effect of DMARDs starts)
what treatments when remission is achieved
gradually withdraw treatments
what is the management pathway for RA
aspirin/ NSAIDs \+ steriods \+DMARD 1 \+DMARD 2 \+DMARD 3
why is aggressive treatment of RA important
stops disease progression- why its essential to diagnose and treat early
how can steroids be given in RA
orally, IA (intra articular) or IM
when steroids be given IA
if fewer than 5 joints involved
name three DMARDs
methotrexate (main one)
sulfasalazine
hydroxycholoquine
(combo therapy with all three)
also have leflunomide, gold injection, penicillamine, azathioprine
what must be give 24 hours after methotrexate
folic acid
what is the route of methotrexate
parenteral
what dosage of methotrexate
start at 15mg/ week then increase
max dose 25mg/week
what precautions should be made when on DMARDs
regularly monitor LFTs and FBCs
teratogenic effects- advise contraception
what are the risks of DMARDs
pneumonitis (methotrexate)
bone marrow suppression
live function derangement
infection
what are biologic agents and when are they used in RA
e.g. anti TNF agents (-mabs), t cell blocker, B cell depletor, IL-6 blocker, JAK 2 inhibitor
dont give to patients already prone in to infection
rationed as very expensive
only when no response to DMARDs and DAS28 score greater that 5.1 on two occasions 4 weeks apart
what is co prescribed by biological agents
methotrexate
what should you screen for and avoid when using biological agents
latent/ active TB, hep B and C, HIV, varicella zoster
avoid live attenuated vaccines
what are the complications of untreated RA
joint damage and deformities
how is cardiovascular disease risk affected by RA
accelerated (risk decreased with DMARDs)
what should be screened for (bone wise) in RA patients
osteoporosis (osteoclasts, post menopausal)
