Rheumatoid Arthritis Flashcards
ACPA pos vs neg
pos-worse effects
neg- never develop full RA
why is ACPA better than RF
RF is seen in other autoab fisorders while ACPA is specfici to RA
it also shows that there will be systemic effectsq
early RA and ACPA
50%
established RA and ACPA
75%
refractory RA and ACPA
85%
HLAII interacts with
CD4+ cells
5 amino acids on HLADR beta chain
increase risk of APCA because they can present cirtullinated proteins to CD4+–>make ACPA protein
ACPA trajectory
begins to appear in serum–>no sx appear–>breach of tolerance occurs–>amplification–>joint targeting–>tissue injury
ACPA and innate immunity
forms immune complexes–>fix complement/stimulate MO–>MO make TNFa and iL6
patho of RA
inflammation of synovium increases cell proliferation
synovium turns to lymphoid tissue
joint destruction-pannus formation
after joint destruction you can have one of..
remission
destruction of cartilage–fibrous, bony ankylosis
weakning,s carring rupture of periarticular structures to decrease fx
Pannus
inflammatory granualtion tissue under the articular cartilage that is made of PMNs and macrophages, generating proteases and synovial fibroblasts that make collagenase and stomeylsin c–>degrading cartilage matrix
where is the most common place for RA
hnads»>feet
symmetry
polyarticular jt involvement in symmetrical distribution–RULE
worse in what time of day
morning
onset of RA
variable
pain increases with
rest
constitutinal sx
loss of strength in hands, fatigue, low grade fever, malaise
what in areas are involved
wrist elbow shoulder hands excpet DIP **loss of symmetry- should question dx
how to score dx
lateral MCP or MTP sequeeze is scored 1-3
wince when shake hands
inability to oppose distal pulp space (claw)
specific PE findings
swelling of 2nd MCP
sublaxation–ulnar deviation because of how we right
swan neck-DIP flex, PIP extension
Boutonniere
swwhy does swan neck happen
synovial erosion of nearby ligs
why does boutonniere occur
bone erosion, forming nodules
if knee- baker’s cyst
risk factor for OA vs RA
OA-wt loss
RA- smoking
what do we check for OA vs RA
1st MCP for OA vs 2nd and 3rd for RA
lab testing RA
anemia chronic disease
increase SED and CRP
synovial fluid- turbid, non-viscuous, demonstartes wbc >1000
RF
IgM to Fc of IgG–seen in 70% of RA, but not specific because 5% of normal population has it in elderly
increase in titer-worse Px
argument for aggressive therapy
damage occurs early-worst in first year
any DMARD is better than placebo-MTX first line
when shouldnt you use hydroxychloroquineee
eye disease
BEST for RA
step up with combos of
methrotrexate
sulfasalazine
mtx/infliximab
hematological extra-articular signs
common-anemia
uncommon-felty’s-leukopenia, splenomegaly, RA (+/- leg ulcers)
dermatologic
rheumatoid nodules-occur following trauma that ruptures vessels at point of impact releasing RF and IC
very uncommon-digital infarcts, livedo reticularis
neurological
common-entrapment neuropathy
uncommon-antlantoaxial subluxation-paraplegic due to spinal cord compression following a surgery because neck was flexed while intubated
very uncommon-peripheral neuropathy
5 forms of pulmonary issues associated with increase RF/ACPA
pulmonary fibrosis nodules pneummoconiosis bronchiolitis obliterans pleural effusion
cardiac
high freq of pericardial effusion, manifesting as pericarditis instead of tamponade
opthalmologic
sicca when RA assocaited with sjorgen syndrome- dysfunction of lacrimal glands because of lymphocyte infiltration
vascular
very uncommon–>secondary to RF
ACPA
specificity
