RA: Rheumatoid Arthritis

USA = Most common Chronic Disease & Most serious form of Arthritis

RA begins in Synovial Membrane  c inflammation of unknown trigger  damages/Irritates the joint membrane  **Transforms IgG to RF (autoantibodies)=> results in inflammatory response **WBC’s found in only in joints of pt’s c RA activated T-cells, macrophages, & monocytes produce CYTOKINES which causes Cartilage destruction and ↑ (of these TNF is significant to RA!) Cytokines – one of large group of PRO’s secreted by some cells (cell2cell communication, amplifies immune response) WBC’s release chemicals that destroy both Bacteria & NL Cells! => Prostaglandins (mediate inflammation) & Leukotriens (produces inflammation) & Collagenase breaks down the collagen – structural PRO base of C. Tissues & c these substances in joints, attracts more WBC’s & the cycle loops making RA a CHRONIC DISEASE General Articular Flare-ups: Generalized & poorly localized, 0 specific joint, A.M. stiffness lasts longer than 1 hr & may be earliest s/s reported  this lasts a long time ā being replaced by a specific localized pain

Stage 2 = Pannus Formation:
**Thickened Synovium that forms a granular substance called PANNUS Pannus invades joint space, covering cartilage & begins to erode it  invading Subchondral bone & its supportive ligaments & tendons  Pannus interferes c NL Nutrition, destroys bone, leads to Necrosis  joint cavity narrows & Motion/Mobility b/comes impaired

S/S’s: of RA:
**Characterized by remissions & Exacerbations  RA’s course is extremely variable(NO 2 pt’s alike)  Some pt’s frequent flare-ups c severe disability & others mild flare-ups c long remission periods & minimal disability

Most forms 0 Life threatening but causes Significant Disability Pt c/o periods of stiffness lasting 2+ hours (or more a day)/day Pain is reason most seek out Dr’s help 50% of ppl(people) dx’d c arthritis are disabled c in 10 yrs from dx made Has SYSTEMIC EFFECTS throughout the body & life threatening b/c it’s a disease of the CONNECTIVE TISSUES (C.Tissues) when RA disease travels  blood & Lymph Systems b/c C. Tissues found in heart valves, BV’s, surrounds & protects body organs, eyes (sclera & Iris)  the RA attacks the body’s own C. Tissues & **Has a preference for Synovial Membranes *REVIEW: Theory on RA on pg 3 PP’s

Remission unlikely p 3 yrs of sustained activity of RA

Stage 3 – Fibrous Ankylosis

(immobility/fixation of a joint) **Tough, fibrous CT replaces the Pannus & occludes joint space  more pronounced cartilage as it dstructs Bone  now, adhesions b/w joint surfaces are present  definite movement limitation  Joint deformity d/t SUBLUXATION: a partial ABN’L separation of the joint’s articular surfaces  weakened tendons & ligaments allow the joint to slip or partially dislocate Stage 4 – Bony Ankylosis: The fibrous tissues Calcifies & total Joint Immobilty results

Diarthroidial joints (free moving) are primarily affected  joints which 2 bones come together to form a joint c a cavity b/w them  cavity forms a joint capsule  cartilage found at ends of bone  joint cavity is lined c Synovial Membrane  Synovial membrane secretes S.F.  S.F. lubricates the joint & allows for smooth movement

RA – ACUTE FLARE-UPS: Localized:
Confined to joints/Articular (affected joints feel sponge-like, boggy, swollen, tender, warm)  very painful joint movements Small Joints are affected first, stiff & achy Joints affected bilaterally & Symmetrically in RA. *B/W Acute Flare-ups: Stiffness & **Achiness last More than 60 mins p getting up in a.m. & **Achiness is UNRELIEVED c REST

FRANK – articular inflammation= Joint swelling, pain, redness, warmth, & Tenderness
Pain 2°/t Cartilage degeneration  areas of exposed bone rubs against ea. Other  may develop fissures (bone cysts caused by excessive inflammatory exudate) & may b/come draining fistulas –communicating c the skin Joint Swelling: affects all joint, primarily affects hands, wrists, elbows, ankles, knees. Hands dev’lop characteristic FUSIFORM Appearance

So, Joint swelling 2°/t inflammation of synovial membrane, or Joint swelling 2°/t New bone formation -- bone spurs or Joint swelling 2°/t Tissue hyperplasia Muscles: Atrophy 2°/t pain & disuse & Spasms contribute to deformity of involved joint Tendon sheaths: Inflammation particularly in wrists RHEUMATOID NODULES: Classic RA Feature!  aggregates of inflammatory cells around a center of cellular debris: may dev’lop near joints, over bony prominences & along extensor surfaces in subQ tissues

SYSTEMIC: Extra-articular: Effects Weight loss, anemia, fatigue, anorexia Lung: pulm -onary fibrosis, pleurisy; RA can effect – Blood Vessles Vasculitis KIDNEY- Nephrotic Synd or Kidney failure Heart-myocarditis, pericarditis EYE- episcleritis, iritis TMJ- can’t open joint  diff c eating Spinal- usually cervical & subluxations may lead to paralysis or death

Pharmacology: Corticosteroids **Lowers pt Immunity & Increases their chances for Infx’ns; avoid LIVE VIRAL VACCINES Steroids are reserved for use when symptoms persist p less potent antiinflammatory Rx’s have been tried

Steroid Administration: 2 methods Intra-articular: fluid removed from the joint & Cortisone is injected Local action on injected joint & effects last weeks  Months Sytemically: given PO, but IV route also Effect is to Suppress inflammation

Antimetabolic Rs’s: Chemotherapy Rx’s Suppress the immune response, is given in smaller doses than ca therapy, new approach is to give early to arrest Joint damage MONITOR: KIDNEY & LIVER toxicity, aplastic anemia Methotrexate: no touch c out gloves on!! Is RX of choice for early active RA, given PO or Injx’n once per week, (NO ETOH/little ETOH may cause LIVER DAMAGE); cause birth defects **pt’s c liver, heart, kidney or lung prob’s are NOT candidates RN pt MGMT of RA: Balance day ċ “rest & exercise” Stress MGMT Adequate Nutrition Use of assistive devices to ↓ Stress placed on joints ****PRONE POSITION maintains proper Body alignment/Hip flexion ċ little joint movement & PILLOWS @ Sides and FEET against footboards to avoid Contractures (a permanent shortening (as of
muscle, tendon, or scar tissue) producing deformity or distortion)

Pharmacology: leflunomide (Arava) Inhibition of DHODH enzyme b/c of its activity in autoimmune process ċ RA pt’s * inhibits the disease progression & joint damage **Monitor blood q month initially


The Biologic Response Modifiers Anti-TNF drugs:

Cont’d: Pharmacology:
Response Modifiers

The Biologic

Anti-TNF drugs: **Anti-TNF’s are Frequently given ċ METHOTREXATE! These med’s are often reserved for RA pt’s ċ NO Response to the other arthritis meds! Serious SE’s: fatal infections, blood dyscrasias (Imbalance of Blood components) & lymphoma Rem.: Trail Rx’s or antidepressants (the TCA’s) are given

*Ậ trx’ting these pt’s give TB Test b/c of their lowered immunity *Etanercept (Enbrel), Remicade, Humira are anti-TNF meds therefore used in RA b/c *TNF plays a role ċ Inflammation: ċ RA **BRM’s (Biologocial Response Modifiers)  Give pt a TB TEST!!

PHYSICAL THERAPY: Goals: to relieve symptoms, joint destruction, maintain joint & muscle fx’n, promotes independence & quality of life Treatments: exercise regimen of ROM on the unaffected jointsHeat therapy (to ↓ muscle spasms, pain, stiffness; only for 15-20 mins each time to avoid tissue destruction)Cold therapy: for its analgesic effects & left on 15-20 mins each time to avoid tissue destruction Splints: used to prevent deformities/ progression of deformities; most custom made to stabilize joint in anatomical position

Non-Pharmocological Interventions: Apply splints to inflamed joints & select clothing ċ VELCRO fasteners, apply

Surgical Interventions: Joint replacement when disease Synovectomy progresses and all else fails **Removal of SYNOVIAL MEMBRANE Most common joints replaced = THR & TKR however most any joint can be  allows for regeneration Moist heat, replaced (regenerates in 60-90 days) **during remission may encourage RA pt to Only effective if done in Stage I (b/c swim in warm pool synovium thickens in this stage) relief of persistent joint inflammation, option when RX therapy fails Document is set-up as follows: “Yellow Highlight” is for columnar headings, “Powder Blue Highlight” is for Stressed items from lecture COX-1 = Houspekeeping fxn’s & is the GOOD COX b/c beneficial actions (suppressions pain/inflammation & lwr’s fever)(ex is ASA= initial choice for RA!; Salicylism= when ASA levels climb ↑’r than 2x’s tx’tic levels (200mcs) & severe toxicity at 400mcg’s: (S/S’s= Tinnitus, sweating, HA * dizziness, acid/base distubancs), children – Reye’s Syndrome (chicken pox/Flu), Irreversible inhibition COX-2 = for tissue injury sites/sensitizes receptors to painful stimuli, is the BAD COX—(ex. Ibuprofen, Aleeve, Toradol, Indocin, Advil, Motrin)  Celebrex & Vioxx Tylenol =Not an NSAID; used for Analgesic & antipyretic properties but devoid of clinically useful anti-infalmmatory/antirheumatic actions. ~2 hr plasma half-life, SE c severe liver damage **Relief of pain & fever, ok for kids BUT 0 useful c trxt’ing ARTHRITIS! OD S/S’s (EARLY signs = N&V, diarrhea, diaphoresis, ABD’l discomfort); to lwr risk of liver damage – use Mucomyst c Tylenol converts toxic metabolite to a nontoxic form & provides protection c in 24hrs of administration shortly p poisoning occurs. 3 adverse E’s (gastric ulceration/suppression of platelet aggregation & renal failure)

0 = Non, not, none; SF = synovial fluid, Rem= remember; c = with, tx = treatment (tx’y=therapy; trx’t = treatment; trxt’ing = treating)
Eberhardt 6/08

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