rheumatoid-arthritis by dandanhuanghuang

VIEWS: 7 PAGES: 2

									                                                                             RHEUMATOLOGY—1
                                                              Conditions that  Rheumatoid Factor:
   RHEUMATOID ARTHRITIS                                       Rheumatic dz: RA, SLE, and Sjogren's syndrome
                                                              Chronic bacterial infections: SBE, Leprosy, Tb, and
Chronic inflammatory disease with symptomatic large
                                                                  Syphilis
    and small joint distribution.
                                                              Viral dz: Rubella, CMV, EBV, influenza, HBV and
Pathophysiology                                                   HCV
Main events contributing to the pathogenesis of               Parasitic dz
    rheumatoid arthritis:                                     Chronic inflammatory dz: Sarcoidosis, periodontal dz,
  Influx of inflammatory cells including neutrophils,            pulmonary interstitial dz and liver dz
    lymphocytes, plasma cells, and macrophages into           Mixed cryoglobulinemia
    synovium                                                  Hypergammaglobulinemic purpura
  Activation and hyperplasia, respectively. Of the
    resident inflammatory cells and synoviocytes              Other Labs:
  Destruction of cartilage and bone by the synovial          ESR:  in nearly all pts with active dz.
    pannus.                                                   Anemia: Normochromic, normocytic. Decreased
Cytokines are involved in one way or another in all three        production.
    events. These include but are not limited to, Il 2, 6,    Diagnosis:
    8, TNF, Vascular Endothelial Growth Factor and            Presence of 4 or more of these criteria must be present
    many others. In another group of chronic                      for >6 weeks are required for a “definite” diagnosis
    inflammatory joint diseases collectively called               of RA.
    spondyloarthropathies (including psoriatic arthritis,     1) Morning stiffness
    ankylosing spondylitis and Reiter’s syndrome), the        2) Arthritis of three or more joint areas
    inflammation is usually centered at the sites of          3) Arthritis of hand joints: PIP, MCP or wrist.
    insertions of ligaments onto bones (entheses). In         4) Symmetrical soft tissue swelling.
    inflammatory arthritis, the synovium is the primary       5) Rheumatoid nodules
    site of involvement; the articular cartilage and bone     6) Serum rheumatoid factor
    are secondarily involved.                                 7) Radiographic changes: erosions and/or periarticular
Compared to OA, RA is considerably more destructive               osteopenia in hand or wrist joints
    to the joints with much less repair. Thus, ankylosis
    is frequent while osteophytes are rare. Also, the         Prognosis:
    inflammation involves periarticular soft tissues, i.e.,   Course is variable and individual.
    joint capsule, tendons, and ligaments and the             Rate of progression toward joint destruction and
    clinical indicators of an inflammatory process are            disability is proportional to:
    much more evident compared to osteoarthritis.               intensity of inflammatory and proliferative reactions
Compared to OA, Amyloidosis is not frequent and when              w/in the joints
    it occurs is mostly due to fibrosis and not bony            persistence of dz over time.
    ankylosis.                                                Most important prognostic factors for destructive
Clinical Presentation:                                            rheumatoid dz:
History: Ask min of AM stiffness and relationship to            Strongly (+) RF
    activity and stress.                                        Presence of rheumatoid nodules
  RA  pain and stiffness improved with mild                   Extra-articular manifestations of rheumatoid dz
    activity but stressing joints remains painful.                such as pericarditis, pleuritis, scleritis, and
  OA  pain and stiffness worse with activity.                   vasculitis.

Articular Manifestations:                                     Current treatment strategies are to be very aggressive
Generalized stiffness esp after inactivity.                       very early in the dz. Bony erosions and joint space
Symmetric arthritis: characteristic involvement of PIP            narrowing occurs and progresses most rapidly
    and MCP. DIP are rarely involved.                             during the first 2 years of the dz.
Synovitis of wrist: Carpal tunnel syndrome
Grip strength and ROM:  by pain or tightness of joint          ADJUNCTIVE TREATMENT
    capsule because of inflammation, joint deformities,       These drugs help to relieve the pain caused by
    subluxation, fibrosis, and contractures.                     inflammation in the joints, but do not change the
Joint effusions                                                  natural course of RA. Are useful in the short term,
Baker’s cyst: hypertrophy of gastroc bursa.                      but the goal is to control the dz and not make these
                                                                 adjuncts needed.
Extra-articular Manifestations:                               NSAIDS
Constitutional symptoms: weakness, easy fatigability,
                                                              Used for pain control as an initial therapeutic goal.
    anorexia, and weight loss.
                                                                  Without such control patients may become
Rheumatoid nodules: Extensor surfaces and over
                                                                  discouraged and noncompliant.
    pressure points. # of nodules does not correlate
                                                              NSAIDS may be supplemented with acetaminophen for
    w/severity of dz.
                                                                  additional analgesia.
Rheumatoid vasculitis: Can affect any organ. Occurs in
                                                              When NSAID medications are used continuously, the
    pts w/severe dz and  circulating RF. In the skin           addition of misoprostol or other GI agents is
    can get palpable purpura, & vasculitic ulcers
                                                                  indicated for most.
Eyes: Scleritis (deeper layers and more serious) and
    episcleritis (mild and transient). Usually in pts         Corticosteroids
    w/long standing dz and nodules.                           Used in low dose oral form for bridging control while
Labs:                                                             waiting for DMARD’s to take effect.
Rheumatoid Factor: Should be ordered if physical
   findings document synovitis compatible with RA.                DISEASE MODIFYING Tx
  IgM antibody to the Fc portion of IgG. (+) is not          Definition: Tx that changes the natural course of RA.
   necessary for diagnosis, but RF is found in ~ 75%              These drugs do not exert anti-inflammatory effects,
  titers correlate w/systemic dz and more severe dz              so NSAIDS must be continued while being used.
Need to relate results to pretest probability of RA.              Benefits are delayed for weeks to months.
   Should not be used as screening test in pts with           Methotrexate:
   inflammatory arthritis.
2—RHEUMATOLOGY
Gold standard for efficacy and documented reduction in
    joint damage.
Effects w/in 4 weeks and plateau at ~ 6 mo. ~ 80% will
    experience moderate to excellent symptomatic
    benefit from Tx, but remission is rare.
Persistent activity supplemented with Anti-TNF drugs
    (Etanercept [Embrel], Infliximab [Remicaide]) or
    Leflunominde.
Methotrexate add-ons/alternatives:
Soluble TNF-alpha Receptor-Fc Fusion Protein:
Etanercept (Embrel): Inhibits binding of TNF- to its
   receptor. Also used in pts w/poor response to MTX.
   Possible future role in early RA.

Infliximab (Remicaide): Chimeric mouse/human anti-
    TNF monoclonal antibody. Lead to  in pain,
    swelling, and tenderness of joints. Approved for pts
    that have inadequate response to MTX alone.
Leflunomide: Indication in pts with poor response to
     MTX or instead of MTX when MTX poorly
     tolerated. Inhibits pyrimidine synthesis pathway
     that is in low numbers in activated T and B cells 
     inhibition of T and B cells.
Cyclosporine: Second line drug after MTX found
     unacceptable. Inhibits activation of CD4 T-cells.
     Some improvement w/in 3 to 6 weeks after
     initiation.
Other drugs:
Minocycline: Used in mild RA. Tetracycline Abx
    demonstrated to superior to placebo. Efficacy may
    be less than that of HDC and/or oral gold.
Sulfasalazine: Used for milder dz. Within 4 to 12
    weeks, most pts experience some improvement.
Hydroxychloroquine: Used in mild RA with no poor
    prognostic factors. Response to therapy is delayed
    for 3 to 6 mo w/plateau at ~ 9 mo.
Gold Compounds: Efficacy questionable. Short-term
   efficacy comparable to MTX, but long-term gold
   loses its effectiveness over time. Subset of patients
   (young women with early dz) experience significant
   dz control and/or remission with gold therapy.

								
To top