RA Flashcards
Reumatoid arthritis characterized by what
systemic double join involvement
age of onset RA and gender
30-50 years
more common in females
shortens life span
race considerations in RA
no discrimination
what to consider to see if genetic?
MHC typing to get HLA level
etiology of RA
unknown
RA has synovial space in joints infiltrated with what
inflammatory cells
(macrophage, t cells, plasma cells)
what is pannus
inflamed proliferation synovium
what do the inflammatory cells do once they invade synovial
release cytokines that lead to cellular proliferatiion and death
what does a pannus do?
invades healthy cartilage and bone and produces erosions that destroy joint
clinical presentation of RA
stiffness and muscle ache - joint swelling
- fatigue
- weak
- loss appetite
- fever
clinical criteria for diagnosis of RA
score of 6 or more points
based on type of joint and number of joints involved
most common joints in RA
hands
wrists
feet
common joints in OA
hands
knee
hip
not as common places for joint inflammation in RA
elbows
shoulder
hip
ankle
knee
reumatoid nodules location
hands
elbow
forearm
reumatoid nodules when to treat
only if symptomatic
usually no intervention required
vasculitis symptoms
inflammation of small supervicial blood vessels
stasis ulcers
infarction leading to necrosis
pulmonary symptoms RA
pleural effusion
pulmonary fibrosis
inflam of arteries and lungs (pnemonitis)
ocular symptoms of RA
inflam of eye, nodules on sclera
keratconjunctivitis sicca - Sjorens syndrome
itchy dry eyes
cardiac effects RA
increase risk CV mortality
pericarditis
conduction abnormalities
myocarditis
Feltys sx RA
splenomegaly - inflamed spleen
neutropenia
additonall disease states that could happen from RA
lympadenopathy
renal disease
thrombocytosis
anemia
(could be from drugs taken)
erythrocyte sedimentation rate and C reactive protein used for what
to see if meds working, disease progression
both non-specific to RA
rheumatoid factor used for what
most patients are RF +
specfic antibody for IgM
higher titer = poorer prognosis
Anti-CCP or ACPA used how
high specificity
marker of poor prognosis
antinuclear antibodies (ANA)
suggest autoimmune disease
more suggestive of SLE
what is joint aspiration
take out fluid from joint to measure
turbid
WBC increased
glucose decreased
radiographic images used how
evaluate disease progression
what increases risk of poor prognosis
elevated CRP and ESR
RF high titers
elevated Anti-CCP / ACPA
erosions on Xray
duration of disease
swelling > 20 joints
goals of therapy
relieve symptoms
preserve function
prevent damage
control extra-articular manifestations
non-pharm treatment RA
rest
weight reduction
surgery
PT/OT
splints/prosthetics
support groups
education
adjunct therapies for RA
NSAIDs
corticosteroids
NSAIDs help with what
pain, swelling, stiffness
DO not alter disease progression
NSAIDs and coritcosteroids as monotherapy?
NO, use with DMARDs
NSAIDs dosed at what
anti-inflammatory doses
if sulfa allergy, what NSAID can we not use?
celecoxib
corticosteroids used for what
anti-inflammatory and immunosuppressive
when could we use corticosteroids?
acute flares
extra-articular manifestations
dose goal for steroids
physiological dose to reduce adverse effects
do not use intraarticular injections how freuntly
more than every 2-3 months
short term side effects corticosteroids
hyperglycemia
gastritis
mood changes
increased BP
long term side effects corticosteroids
aseptic necrosis
cataracts
obesity
growth failure
osteoporosis
HPA suppression
baseline monitoring for corticosteroids
BP
BG
maintenance monitoring for corticosteroids
BP
BG
every 3-6 months
what is a DMARD
disease modifying anti-reumatic drug
what can DMARDs do
decrease/prevent joint damage
preserve joint integrity
onset of action DMARDs
6 months, takes awhile
conventional synthetic DMARDs still used
methotrexate
sulfasalazine
hydroxychloroquine
leflunomide
DMARD of choice
methotrexate, best long term outcome