Rheum 1 - RA Flashcards
What is RA
Symmetric inflammatory polyarthritis with significant morning stiffness
Thought to be an immune mediated process leading to joint inflammation and destruction
RA vs. OA for the what is it
OA - more mechanical - more wear and tear - the morning stiffness is not as significant
RA - immune system is over active so a lot of meds are immunosuppressants
ACA criteria for diagnosis of RA - need how many for how long
Need at least 4 of the criteria and must be present for more than 6 weeks
ACA criteria diagnosis for RA
1 Morning stiffness typically lasting more than 1 hour
2 Swelling of more than 3 joints
3 Symmetric distribution
4 Involvement of hand joints - esp wrists, MCPs, and PIPs, sparing DIPs
5 Pos RF (80% of pts with RA)
6 Rheumatoid nodules on extensor surfaces, esp the olecranon
OA vs. RA for joints involved
OA - CMC, PIP, DIP
RA - MCP, PIP
What causes RA?
We really don’t know!
What has been studied as a cause for RA?
Infectious agents - mycoplasma, EBV, cytomegalovirus, parvovirus B19
Occupational and SES
Smoking - recent studies suggest strong association
Who does RA affect?
1% of the population
3:1 W to M
Incidence increases in adulthood and continues through 70s+
Genetics account for 15% of risk and other 85% is environmental factors
Lab studies for RA
RF
Anti CCP
Inflammation - CRP, ESR
CBC, ALT/AST, Albumin, Creatinine, Alk phos, UA
Lab studies - Rheumatoid factor
More than 13 ng/mL is considered seropositive
Just because someone has positive RF though does not mean that they have RA (other diseases can have + RF like Hep C, TB, Symphilis, SLE, myositis)
30% with RA will not develop a + RF
Lab studies - Anti CCP
Anti cycle citrullinaed peptide
More specific to RA - if this is positive, they definitely have RA
Levels of over 20 ng/mL are considered pos
Might be present months prior to onset of clinical symptoms
Lab studies - Seropositive vs. seronegative RA
Seropositive denotes RA patients with a positive RF
40% of seronegative RA patients are anti CCP positive
Lab studies - if in flare will see what
Increase in CRP (C reactive protein) and ESR (Erythrocyte sedimentation rate)
Joints commonly involved in RA
MCPs PIPs Wrists MTP joints Cervical spine (NOT LUMBAR) Hips Knees Ankles TMJ
Course of RA
Some experience mild disease and have spontaneous remission
Most suffer a chronic course with intermittent disease flares and progressive joint deformities
Synovitis
When synovial fluid is produced in excess amount we get synovitis - excessive synovial fluid in joint capsule
Differentiate with OA - touch - OA will be hard because it is bony hypertrophy
Ulnar deviation
Because of joint erosions
Deformities that can be seen with RA
Synovitis Ulnar deviation Telescoping Swan neck and Boutonniere Hallux valgus
Radiographic changes
Need to get a baseline and every 1 to 2 year of the hands and feet
Erosions can be seen - 70% develop them in the 1st 2 years
Osteopenia (Classic for RA)
Loss of articular cartilage (seen with OA too)
RA vs. OA changes in the knee
RA will see medial and lateral are equally affected
OA will see more medial affected
RA - affects other than the joints
Neuro - Nerve entrapment, cervical spine instbaility
Cardiac - pericardial effusions, pericarditis
Renal/GI - amyloidosis
Hematologic - microcytic anemia
Skin - nodules, vasculitic ulcerations
Ocular - sicca dry eye, scleritis
Pulmonary - fibrosis, nodules (multiple)
Treatment of RA
Corticosteroids
NSAIDs
DMARDs
Biologic therapy
Treatment of RA - corticosteroids
Rapidly acting but do NOT affect disease course
Used for flares or as chronic therapy
Bridge therapy - can help control symptos while waiting for action of second line agents
Burst and taper can be given (prednisone)
Oral dose pack tapering - Methylprednisolone
Intramuscular steroids
Intra articular joint injections
Treatment of RA - corticosteroids - side effects
Short term = mood change, sleep is hard
Long term = bone loss, bruising, cataracts, inc appetite/weight gain, buffalo hump, moon face
