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
Treatment of RA - NSAIDs
Effective for swelling, pain, stiffness
NO disease modification
OTC - ibuprofen, naproxen Na (Aleve)
Rx - Sulindac, Meloxicam, Nabumetone
Treatment of RA - NSAIDs - side effects
GI - ulceration, performation, dyspepsia
Renal - hypertension, decreased GFR
CV - CHF
Antiplatelet effect
Pre medication screening - prior to starting meds need
Chest x ray - look for evidence of TB, infection, nodules
Heb B and C screen
TB test
Immunizations
Vaccines recommended prior to therapy - Influenza, pneumonia
NOT live vaccines if they are on immunosuppressive drugs
DMARDs
FIRST LINE - this is where they turn first - long term meds for these patients
Not all pts respond to therapy
Therapy may slow down but not always prevent joint damage
Frequently used in combo to improve efficacy
Have potential for significant untoward effects
Gold standard DMARD
Methotrexate!
Gold standard for tx of RA
Dose in 2.5 mg tablets - once weekly or injection
NO ALCOHOL use while on it, also with preg is cat X
Other common DMARD to know
Arava (Leflunomide)
Dosage 10-20 mg daily
Contraindicated in pregnancy
Side effects of DMARDs - methotrexate and leflunomide
Neutropenia, liver damage, alopecia, oral ulcerations, dirrhea, nausea, infection, myelosuppression
Other DMARDs used
Sulfasalazine Hydroxychloroquine Azathioprine Cyclosporine Minocycline/Doxycycline Gold salts Cyclophosphamide Penicillamine
Biologic therapy for RA
TNF inhibitors
Injectable or IV
Biologic therapy for RA - TNF inhibitors - Injectable
Enbrel (Etanercept)
Humira (adalimumab)
Cimzia (certolizumab pegol)
Simponi (golimumab)
Biologic therapy for RA - TNF inhibitors -IV
Remicade (Inliximab) Simponi Aria (golimumab)
Biologic therapy for RA - TNF inhibitors - Other
Rituxan (rituximab)
Orencia (abatacept) - T cell inhibitor
Actemra (Tocilizumab)
Xeljanx (Tofacitinib)
Biologic therapy for RA - TNF inhibitors -Black box warnings
Opportunistic infections - Histoplasmosis, TB
Malignancies - Lymphoma, lung cancer
Biologic therapy for RA - TNF inhibitors -Risks
Inc risk of infections Infusion rxns with IV Remicade Avoid live vaccines Major elective surgeries should be avoided 2 wks before and after TNF therapy Avoided in preg Monitor for demyelinating disease
Nonparmacologic therapy
PT
OT
Alt med - Chiropractic, acupuncutre, herbal remedies, vitamins
ACA criteria for remission
5 or more of the following must be met: 1 Morning stiffness less than 15 min 2 No fatigue 3 No joint pain (by hx) 4 No joint tenderness or pain in motion 5 No soft tissue swelling in joint or tendons 6 ESR F less than 30, males less than 20
Pregnancy and RA
75% improve or go into remission during preg
Controversy over what RA meds can be used - Prednisone is probably the safest of them
Prognosis for RA
Increase mortality rate - reduced survival by 10+ years
Most common causes of inc mortality = 2x inc rate of MI, Heart failure, and CV disease
Inc rate of certain CA including lymphoma
Serious infections
Related conditions - Palindromic Rheumatism
Pts develop recurrent onsets of acute, self limited arthritis
Attacks usually last hours to a few days and may involve any set of joints - is usually a single joint stays there and then migrates to another single joint
Joint damage and systemic s/s are rare
Many later progress to RA
Tx similar to RA
Related conditions - Felty’s syndrome
Triad of RA, splenomegaly, leukopenia
Occurs in pts with long standing seropositive RA
Manifestations = recurrent bacterial infections, LW ulcers, thrombocytopenia
Aggressive tx of underlying RA is the goal of tx
Related conditions - Adult onset still’s disease
Adult version of JRA
Onset age between 16-35 with 10% after age 50
Daily spiking fevers that are high and occure at the same time each day
Chronic polyarthritis
Rash evident with febrile episodes (trunk, neck, extrem)
Tx = NSAIDs, Prednisone
Drug tx
DMARDs = first line - methotrexate
?
Biologic agents are next step up (prevent disease from getting worse)
