Autoimmune disorders.RA, OA, Gout

Autoimmune Disorders: Rheumatoid Arthritis, Osteoarthritis, &

Gouty Arthritis Gouty Arthritis

Maria Carmela L. Domocmat, RN, MSNInstructor, Curative and Rehabilitative Nursing Care II

School of Nursing Northern Luzon Adventist College

Rheumatic Disorders

Comprise autoimmune and inflammatory disorders ‘the primary crippling disease”Inflammation of jointInflammation of jointPrimary reason for work-related disability Leading cause of disability among 65 yrs old and above

Maria Carmela L. Domocmat, RN, MSN

What causes autoimmune disease?

http://www.medscape.com/content/2000/00/40/87/408750/art-mrc4856.lymp.fig2.gif

Certain variants or mutations in the MHC genes may result in abnormal MHC proteins


Reaction to Self

Occurs when the immune system sees “self”

antigens as “nonself”

may be due to genetic factors, infectious agents, may be due to genetic factors, infectious agents,

gender, and age

the autoimmune response results in tissue

damage

Some damage occurs in only one or a few organs, in

other cases it may be body-wide (systemic)Maria Carmela L. Domocmat, RN, MSN

Reaction to Self

~ 3.5 % of people have autoimmune diseases

On average, women are 2.7 times more likely to

develop these diseases than men

most have no known cause or cure

treatment is aimed at controlling symptoms


Why does the immune system attack the body that it’s supposed to protect?

failure to recognize some cells as “self”in rheumatic fever, the streptococcus antigen is very similar to a protein in heart tissue, so the body mistakenly identifies heart tissues as foreign

cells seen as foreign are attacked and destroyedcells seen as foreign are attacked and destroyedmay be only a few select cells or organs (organ-specific) – e.g., multiple sclerosis, juvenile diabetes, rheumatic fevermay be systemic - e.g., systemic lupus erythematosus, rheumatoid arthritis




Rheumatoid Arthritis (RA)

chronic systemic autoimmune disease- anti-self antibodies that react with the constant regions of other

antibodies (rheumatoid factor)

onset of disease occurs most often between the ages of 25-55

women are 3 times more likely to develop this than menwomen are 3 times more likely to develop this than men

symptoms include weakness, fatigue, and joint paininfections, hormones and genetic factors may be involved

X-ray shows severe arthritis affecting the joints and limiting mobility


Rheumatoid arthritis (RA) affects peripheral joints and may cause destruction of both cartilage and bone. The disease affects mainly individuals carrying the DR4 variant of MHC genes.


Treatment





ACR Clinical Classification Criteria for Rheumatoid Arthritisusing history, physical examination, laboratory and radiographic findings:


ACR Clinical Classification Criteria for Rheumatoid Arthritis



ACR Clinical Classification Criteria for Juvenile Rheumatoid Arthritis

GENERAL CLASSa. Persistent arthritis of at least six weeks duration in one or more jointsb. Exclusion of other causes of arthritis (see list of exclusions+)exclusions+)onset subtypes -determined by manifestations during the first six months of disease although manifestations more closely resembling another subtype may appear later


ACR Classification Criteria for Determining Progression of

Rheumatoid Arthritis*These criteria describe either spontaneous remission

or a state of drug-induced disease suppression.

Rheumatoid Arthritis



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Initial Laboratory work -up

Complete blood countComprehensive metabolic panelUrinalysisSedimentation RateSedimentation RateRheumatoid FactorAnti-nuclear Antibody


Chemistries

normal with the exception of a slight decrease in albumin and increase in total protein reflecting the chronic inflammatory process. Renal and liver function should be checked prior to instituting therapy.


Hematology

mild anemia with hematocrit values in the range of 30 - 34% occurs in approximately 25 to 35% of patientsIn most cases, the reduced red cell mass is caused by the anemia of chronic disease, a normocytic-normochromic process characterized by a low concentration of serum iron, a low serum iron-binding capacity, and a normal or increased serum ferritin concentration. occasionally true iron deficiency anemia can develop secondary to intercurrentoccasionally true iron deficiency anemia can develop secondary to intercurrentblood loss often from gastrointestinal (GI) bleeding due to NSAIDS.

Patients should be monitored closely for symptoms of GI bleeding and consideration must also be given to other causes of GI blood loss such as colonic lesions.


white cell count platelet count

usually normal can be mildly elevated secondary to

usually normal but thrombocytosis occurs in response to

Hematology

secondary to inflammation.

occurs in response to inflammation. Drug reactions and Felty's syndrome are rare causes of leukopenia or thrombocytopenia


Hematology

Increased erythrocyte sedimentation rate (ESR)


Serology

(+) RFRheumatoid factors

are autoantibodies directed against IgG

A positive test for rheumatoid factor (RF) A positive test for rheumatoid factor (RF) pathognomonic of rheumatoid arthritis


Radiology

early in the disease show nothing other than soft tissue swelling.

periarticular osteopenia may develop. With progression of diseaseWith progression of disease

narrowing of the joint space is caused by loss of cartilage, and juxta-articular erosions appear, generally at the point of attachment of the synovium.

end-stage diseaselarge cystic erosions of bone may be seen. Bony proliferation may occur because of degenerative changes that follow inflammation.


Clinical manifestations



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Typical visible changes include ulnar deviation of the fingers at the MCP joints, hyperextension or hyperflexion of the MCP and PIP joints, flexion and PIP joints, flexion contractures of the elbows, and subluxation of the carpal bones and toes (cocked -up).


Extra -Articular Disease

Rheumatoid NodulesCardiopulmonary DiseaseOcular DiseaseNeurologic DiseaseNeurologic DiseaseFelty's SyndromeRheumatoid VasculitisSjogren's Syndrome


Rheumatoid Nodules

subcutaneous nodule the most characteristic extra-articular lesion of the disease. occur in 20 to 30% of cases, almost exclusively in seropositive patients. seropositive patients. located most commonly on the extensor surfaces of the arms and elbows but are also prone to develop at pressure points on the feet and knees.


Rheumatoid Nodules

http://images.rheumatology.org/viewphoto.php?imageId=3011201&albumId=75692


Rheumatoid Nodules

Rheumatoid nodules commonly form near the extensor surface of the elbow. They can be fixed to the underlying to the underlying periosteum or can be freely mobile.


Caplan’s Syndrome

Presence of rheumatoid nodules in lungs pneumococcus (noted in among coal miners and asbestos workers)

http://images.rheumatology.org/image_dir/album75692/md_99-05-0096_1.tif.jpg


Cardiopulmonary Disease

There are several pulmonary manifestations of rheumatoid arthritis, including pleurisy with or without effusion, intrapulmonary nodules, intrapulmonary nodules, rheumatoid pneumoconiosis (Caplan's syndrome), diffuse interstitial fibrosis, and rarely, bronchiolitis obliterans pneumothorax.


Cardiopulmonary Disease

On pulmonary function testing, there commonly is a restrictive ventilatory defect with reduced lung volumes and a decreased diffusing capacity for carbon monoxide.

Although mostly asymptomatic, of greatest Although mostly asymptomatic, of greatest concern is distinguishing these manifestations from infection and tumor. Pericarditis is the most common cardiac manifestation.


Neurologic Disease

most common - is a mild, primarily sensory peripheral neuropathy, usually more marked in the lower extremities. Entrapment neuropathies (e.g., carpal tunnel syndrome and tarsal tunnel syndrome) sometimes syndrome and tarsal tunnel syndrome) sometimes occur because of compression of a peripheral nerve by inflamed edematous tissue.


Neurologic Disease

Cervical myelopathy secondary to atlantoaxial subluxation is an uncommon but particularly worrisome complication potentially causing permanent, even fatal neurologic damage.


Felty's Syndrome

is characterized by splenomegalyleukopenia - predominantly granulocytopenia.

rare complication Recurrent bacterial infections and chronic refractory leg ulcers are the major complications.


Rheumatoid Vasculitis

most common clinical manifestations are small digital infarcts along the nailbeds.


Sjogren's Syndrome

a chronic inflammatory disorder characterized by lymphocytic infiltration of lacrimal and salivary glands. leads to impaired secretion of saliva and tears and results in the sicca complex: results in the sicca complex:

dry mouth (xerostomia) dry eyes (keratoconjunctivitis sicca)dry vagina (rare)


Criteria for Diagnosis of Sjögren's Syndrome

Four or more of the following following criteria must be present


Ocular Disease

Keratoconjunctivitis of Sjogren's syndrome is the most common ocular manifestation of rheumatoid arthritis. Sicca (dry eyes) is a common complaint.Episcleritis occurs occasionally and is manifested by mild pain and intense redness of the affected eye. Scleritis and corneal ulcerations are rare but more serious problems.


Keratoconjunctivitis, Sicca


PROGNOSIS


Disability is higher among patients with rheumatoid arthritis with 60% being unable to work 10 years after the onset of their disease. Recent studies have demonstrated an increased mortality in rheumatoid patients. mortality in rheumatoid patients. Median life expectancy was shortened an average of 7 years for men and 3 years for women compared to control populations.


Patients at higher risk for shortened survival are those with

systemic extra-articular involvement, low functional capacity, low socioeconomic status, low socioeconomic status, low education, and prednisone use.


ACR Guidelines for Medical Management of Rheumatoid

Arthritis(updated April, 2002)

Arthritis


http://rezidentiat.3x.ro/eng/pareng.files/image015.gifMaria Carmela L. Domocmat, RN, MSN

Management


The goal of treatment now aims toward achieving the lowest possible level of arthritis disease activity and remission if possible, the minimization of joint damage, and enhancing physical function and quality of life.


� Reduce pain and inflammation

� Protect Articular surface

› Reduction of joint stress

� Maintain function � Maintain function

› ROM exercises

› Physical and occupational therapy

� Surgical intervention


REDUCE PAIN AND INFLAMMATION


Pharmacologic treatment

1. Non-steroidal Anti-inflammatory Agents (NSAIDs)

2. Corticosteroids3. Disease Modifying Anti -rheumatic Drugs 3. Disease Modifying Anti -rheumatic Drugs

(DMARDs)


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NSAIDs and corticosteroids

have a short onset of action while DMARDs can take several weeks or months to demonstrate a clinical effect


NON-STEROIDAL ANTI-INFLAMMATORY AGENTS (NSAIDS)


NSAIDs

major effect - reduce acute inflammation thereby decreasing pain and improving function. have mild to moderate analgesic properties independent of their anti-inflammatory effect. Note: these drugs alone do not change the course of the disease of rheumatoid arthritis or prevent joint destruction.


OTC NSAIDs

Aspirinibuprofen (Advil ®, Motrin®, Nuprin ®) naproxen (Alleve®, Flanax)ketoprofen (Actron, Orudis KT)ketoprofen (Actron, Orudis KT)


Aspirin - oldest drug of the non-steroidal classbut because of its high rate of GI toxicity, a narrow window between toxic and anti-inflammatory serum levels, and the inconvenience of multiple daily doses, aspirin's use as the initial choice of drug therapy aspirin's use as the initial choice of drug therapy has largely been replaced by other NSAIDs.


Prescription NSAIDs include

meloxicam (Mobic®), etodolac (Lodine®), nabumetone (Relafen®), sulindac (Clinoril®), tolementin (Tolectin®),

diclofenac (Cataflam®, Voltaren®, Arthrotec®), diflusinal (Dolobid®), indomethicin (Indocin®), ketoprofen (Orudis®, tolementin (Tolectin®),

choline magnesium salicylate (Trilasate®), flurbiprofen (Ansaid),dexibuprofen (Seractil)

ketoprofen (Orudis®, Oruvail®), oxaprozin (Daypro®), piroxicam (Feldene®).



Drugs for Prevention NSAID-Induced Ulcers

If NSAID-induced ulcers are identified, the following steps have been suggested:Switch to alternative pain relievers.

proton-pump inhibitors (PPIs). misoprostol or Arthrotec. L-arginine

If cannot change drugs, then should use lowest NSAID dose possible



proton-pump inhibitors (PPIs). Can reduce NSAID-ulcer rates by as much as 80% compared with no treatment. omeprazole (Prilosec)esomeprazole (Nexium)esomeprazole (Nexium)lansoprazole (Prevacid),rabeprazole (Aciphex), pantoprozole (Protonix).



Try misoprostol or Arthrotec. If other agents are inappropriate, misoprostol protects against the major intestinal toxicity of NSAIDs. the first drug approved for preventing NSAID-induced ulcers. It is equally or even more effective than some of the PPIs, but it does not heal existing ulcers and has more side effects than does not heal existing ulcers and has more side effects than PPIs. Patients tend to stop using it.

Arthrotec - a combination of an ulcer protective agent called misoprostol and the NSAID diclofenac.


L-arginine supplementan amino acid found in health storesmay help protect against damage from NSAIDs.an alternative agentnot government regulated and more research is needed to confirm its benefits.


Topical NSAIDs

delivered in gels, creams, or patches are proving to reduce arthritic pain and pose less of a risk for gastrointestinal complications associated with oral NSAIDs. diclofenac (Pennsaid, Oxa Sat)eltenac, ibuprofen, or ketoprofen.


$63.07


NSAIDS: COX-2 inhibitor

includes COX-2 inhibitors also effective in controlling inflammation. Only one of these agents is currently available in the United States (celecoxib, Celebrex®) while the United States (celecoxib, Celebrex®) while additional compounds are available in other countries (etoricoxib, Arcoxia®; lumiracoxib, Prexige®).


or COX-2 medications


COX-2 inhibitors designed to decrease the gastrointestinal risk of NSAIDS, but concerns of possible increases in but concerns of possible increases in cardiovascular risk with these agents has led to the withdrawal of two of these drugs from the market (rofecoxib, Vioxx®; valdecoxib, Bextra®).


CORTICOSTEROIDS


Corticosteroids

anti-inflammatory & immunoregulatory activity. PO, IV, IM or can be injected directly into the joint. useful in early disease as temporary adjunctive therapy while waiting for DMARDs to exert their therapy while waiting for DMARDs to exert their antiinflammatory effects.


Corticosteroids


Corticosteroids

also useful as chronic adjunctive therapy in patients with severe disease that is not well controlled on NSAIDs and DMARDs.

Weight gain and a cushingoid appearance(increased fat deposition around the face, redness of the cheeks, development of a “buffalo hump” over the neck) is a frequent problem and source of patient complaints


cushingoid appearance


Prevent osteoporosis due to steroid use

adequate calcium and vitamin D supplementationBisphosphonates

alendronate (Fosamax®)risedronate (Actonel®)ibandronate (Boniva®)

Patients with and without osteoporosis risk factors on low dose prednisone should undergo bone densitometry (DEXA Scan) to assess fracture risk.


Intra-articular corticosteroids(e.g., triamcinolone or methylprednisolone and others)

are effective for controlling a local flare in a joint without changing the flare in a joint without changing the overall drug regimen.


http://www.mayoclinicproceedings.com/content/84/9/831.fullMaria Carmela L. Domocmat, RN, MSN

DISEASE MODIFYING ANTI-RHEUMATIC DRUGS (DMARDS)


Disease Modifying Anti-rheumatic Drugs (DMARDs)

Can alter the disease course and improve radiographic outcomes. DMARDs have an effect upon rheumatoid arthritis that is different and may be more delayed in onset than either NSAIDs or corticosteroids. than either NSAIDs or corticosteroids. when the diagnosis of rheumatoid arthritis is confirmed, DMARD agents should be started.


DMARDs

Methotrexate (Rheumatrex®, Trexall®)Hydroxychloroquine (Plaquenil ®)Sulfasalazine (Azulfidine®)Leflunomide (Arava®)Leflunomide (Arava®)Tumor Necrosis Factor Inhibitors

etanercept (Enbrel®, adalimumab (Humira ®), and infliximab (Remicade®)

T-cell Costimulatory Blocking Agentsabatacept (Orencia®)


DMARDs

B cell Depleting Agentsrituximab (Rituxan®)

Interleukin-1 (IL-1) Receptor Antagonist Therapyanakinra (Kineret®)

Intramuscular GoldOther Immunomodulatory and Cytotoxic agents—

azathioprine (Imuran®), cyclophosphamide, and cyclosporine A(Neoral®, Sandimmune®)


Methotrexate

the first-line DMARD agentHas rapid onset of action at therapeutic doses (6-8 weeks)good efficacygood efficacyfavorable toxicity profileease of administrationand relatively low cost.


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Hydroxychloroquine

an antimalarial drug relatively safe and well-tolerated agent for the treatment of rheumatoid arthritis.have limited ability to prevent joint damage on have limited ability to prevent joint damage on their own, their use should probably be limited to patients with very mild and nonerosive disease.


Hydroxychloroquine

is sometimes combined with methotrexate for additive benefits for signs and symptoms or as part of a regimen of “triple therapy” with methotrexate and sulfasalazine.


Sulfasalazine

Azulfidine®effectiveness - somewhat less than that methotrexate, reduce signs and symptoms and reduce signs and symptoms and slow radiographic damage. given in conjunction with methotrexate and hydroxychloroquine as part of a regimen of “triple therapy”


Leflunomide (Arava®)

efficacy is similar to methotrexate in terms of signs and symptomsviable alternative - failed or are intolerant to methotrexate.


Tumor necrosis factor (TNF) inhibitors

Tumor necrosis factor alpha (TNF) is a pro-inflammatory cytokine produced by macrophages and lymphocytes. found in large quantities in the rheumatoid joint and is produced locally in the joint by synovial macrophages produced locally in the joint by synovial macrophages and lymphocytes infiltrating the joint synovium.TNF is one of the critical cytokines that mediate joint damage and destruction due to its activities on many cells in the joint as well as effects on other organs and body systems.


TNF antagonists

first of the biological DMARDS to be approved for the treatment of RA and have also been referred to as biological response modifiers or “biologics” to differentiate them from other DMARDS such as differentiate them from other DMARDS such as methotrexate, leflunomide, or sulfasalazine.


TNFs or Biological Response Modifiers (BRMs)

Etanercept (Enbrel®) Infliximab (Remicade®)Adalimumab (Humira®)


Etanercept (Enbrel®)

Etanercept is effective in reducing the signs and symptoms of RA, as well as in slowing or halting radiographic damage, when used either as monotherapy or in combination with methotrexate.


Infliximab (Remicade ®)

Infliximab, in combination with methotrexate, is approved for the treatment of RA, and for the treatment of psoriatic arthritis, and ankylosing spondylitis, as well as psoriasis and Crohn’s disease.disease.


Adalimumab (Humira ®)

Adalimumab is a fully human anti-TNF monoclonal antibody with high specificity for TNF.


Anakinra (Kineret™)

a human recombinant IL-1 receptor antagonist (hurIL-1ra) can be used alone or in combination with DMARDs other than TNF blocking agents (Etanercept, Infliximab, Adalimumab). (Etanercept, Infliximab, Adalimumab).


T-cell Costimulatory blockade

Abatacept (Orencia®)first of a class of agents known as T-cell costimulatory blockers.interfere with the interactions between antigen-interfere with the interactions between antigen-presenting cells and T lymphocytes and affect early stages in the pathogenic cascade of events in rheumatoid arthritis.


Intramuscular Gold

Myochrysine® and Solganal®IMhave been replaced by Methotrexate and other DMARDS Methotrexate and other DMARDS as the preferred agents to treat RA. rarely used now due to their numerous side effects and monitoring requirements, their limited efficacy, and very slow onset of action.


Plasmapheresis


Alternative treatmentsglucosamine sulfate chondroitin sulfateareare dietary supplements usually taken in pill form that are thought to protect and possibly help repair are thought to protect and possibly help repair cartilage cells.


NURSING MANAGEMENT


Chronic pain r/t inflammation and swelling from pressure on surrounding tissues, joint deformity and joint destruction

Teach about medsPromote comfort with nonpharmacologic measuresManage stiffnessPromote sleep and rest


Promote comfort with nonpharmacologic measures


Manage stiffness


Promote sleep and rest

Encourage to sleep at least 8 hrs at night, take daily napsPromote a quiet envtProvide warm beverages before retiring to sleepProvide warm beverages before retiring to sleepAdminister hypnotics or relaxants as prescribed


REDUCTION OF JOINT STRESS


Reduction of joint stress

Because obesity stresses the musculoskeletal system, ideal body weight should be achieved and maintained. Rest, in general, is an important feature of management. management. When the joints are actively inflamed, vigorous activity should be avoided because of the danger of intensifying joint inflammation or causing traumatic injury to structures weakened by inflammation.


Readiness for enhanced self-care r/t complex medication schedules, high risk of S/E of meds, health maintenance, and self-care

Promote balanced dietPromote decision-makingPromote hope Promote coping


Self-care

Use china or heavy plastic cup with handle which is easier to manipulate rather than styrofoam or paper cup which may bend or collapse When fine motor activities become impossible –use larger joints or body surfaces

Ex: use palm of hand to press the toothpaste to toothbrush rather than the fingers Use devices – long-handed brushes to brush hair or dressing sticks for facilitite wearing of pants


Reduction of joint stress

urge to maintain a modest level of activity to prevent joint laxity and muscular atrophy. Splinting of acutely inflamed joints, particularly at night and the use of walking aids (canes, walkers) are all effective means of reducing stress on are all effective means of reducing stress on specific joints.


Assistive devices

Computer Keyboard Aid

Arthritic's Pen

Computer Keyboard Aid


Phone & Cup Holder with Hook and Loop Strap


Arthritis in your hands causes your finger joints and knuckles to become stiff and sometimes painful and swollen. Protect your hands by Protect your hands by avoiding pushing, pulling and twisting motions. Avoid making a tight fist or pinching objects tightly.


Instead, use a grasp that aligns your knuckles evenly along the handle of the tool or utensil. This makes grasping the tool more comfortable tool more comfortable and requires less effort to use the tool. For instance, a built-up handle made of foam can make it easier for you to grasp your toothbrush.


For tasks that require you to pinch objects tightly, look for assistive devices that can help you hold the object with less force. For instance, using a special key holder may help you turn key holder may help you turn keys more comfortably without putting strain on your hand. This type of holder aligns your knuckles evenly along the handle of the tool or utensil, allowing you to use a larger grip to turn the key.


Use assistive devices to help you open jars. This spares your fingers from the twisting motion required to open a jar.


To protect your finger joints, avoid tightly pinching with your fingers. For example, use a button aid to help you grasp and aid to help you grasp and fasten buttons on your clothes. Choose clothes with easy-to-close fasteners, such as zippers, large buttons or hooks.


Promote balanced dietGood oral hygiene b4 and after mealsSmall, frequent feedingsHigh-caloric snacksIf with xerostamia – moisten foods, extra fluids with meals meals Eliminate spicy or acidic foodsSit upright to eatTake all meds with food and full glass of water – to ameliorate GI distressUse assistive device if with stiffness


Promote decision-making

Exercise healthy control over the diseaseClient should be able to verbalize cause of illness Educate the client

Increase participation in decision-making Increase participation in decision-making allow as many choices as possibleDecide on own ADL


Promote hope

Avoid false reassuranceHelp set realistic goalsPraise for accomplishments (no matter how small)small)Active listening Be sensitive to changes in mind and affect


Promote coping

The client would be able to integrate disease into the demands of daily living Sign that the client has healthy approach strategiesstrategies

Seek out info and assistanceFind strength through spiritual supportVerbalize feelings and concernsSet goalsExpress positive thoughtsMaintain realistic independence


Signs of less adaptive strategiesAvoidance strategies – ex: denial Excessive sleepingOther passive behaviorsDepression


FATIGUE


Management of Fatigue:

For muscle atrophy – aggressive PT to strengthen muscle and prevent further atrophy


Management of FatiguePrinciples of energy conservation

Pacing activities- do not plan too much activity for one day Allow rest periodsSet priorities – determine which activities are most Set priorities – determine which activities are most important and do them first Obtain assistance when needed – delegate responsibilities balance activity and rest Plan ahead to prevent last minute rushing and stress Learn own activity tolerance and do not exceed it


BODY IMAGE DISTURBANCE


Enhance body image

Body image may be affected by both the disease process and drug therapy

Ulnar deviation, swan-neck deformity, boutonnière deformity, rheumatoid nodules Steroid side effect – cushingoid syndromeSteroid side effect – cushingoid syndrome

Determine client’s perception of the changes and impact of reaction of the SO Most impt Ix – communicate acceptance of the client ; establish and maintain trusting relationship to encourage the client to express feelings


Let the client wear own clothes rather than the hosp gown, brush own hair, use make-up if desiredUse colored hair accessories , nail polish, Use colored hair accessories , nail polish, perfume


SURGICAL INTERVENTIONS


Surgical interventions

Tendon transfer and osteotomySynovectomyArthrodesisJoint arthroplasty or replacement Joint arthroplasty or replacement


Tendon transfer and osteotomy

Nodules or benign bony tumors (exostoses) –surgically removed and flexion contractures surgically relievedOsteotomiesOsteotomies

Excision or cutting through bones


Synovectomy

Surgical removal of synovia – elbow, wrist, fingers, knees


Synovectomy

ordinarily not recommended for patients with rheumatoid arthritis, primarily because relief is only transient. synovectomy of the wrist - an exception

recommended if intense synovitis is persistent despite medical treatment over 6 to 12 months. Persistent synovitis involving the dorsal compartments of the wrist can lead to extensor tendon sheath rupture resulting in severe disability of hand function.


Synovectomy



Arthrodesis

Operation that produce bony fusion of joint used for clients with bone loss after joint infection , tumors, musculoskeletal trauma, paralysis paralysis Immobilize the joint but eliminate some discomfort or arthritic process Ankle - most common


Joint arthroplasty or replacement

particularly of the knee, hip, wrist, and elbow, are highly successful. Arthroplasty of the metacarpophalangeal (knuckle) joints also can reduce pain and improve function.


Hip Replacement



Surgical intervention


Surgical intervention

Other operations include release of nerve entrapments (e.g., carpal tunnel syndrome)arthroscopic proceduresremoval of a symptomatic rheumatoid nodule. -removal of a symptomatic rheumatoid nodule. -occasionally


Complementary/ Alternative therapies

Pain relief – hypnosis, acupuncture, magnet Good nutrition

Omega-3 fatty acidsFound in coldwater fish (salmon, sea bass, tuna)May help reduce inflamBut amount needed is impractical to human consumption

Fish oil capsules


Complementary/ Alternative therapies

Antioxidant vitamins (A,C, E) to help maintain normal function of the immune system Trace elements for joint health

Zinc, Selenium, Copper, Iron


Osteoarthritis

associated with the aging process and can affect any joint. The cartilage of the affected joint is affected joint is gradually worn down, eventually causing bone to rub against bone. Bony spurs develop on the unprotected bones, causing pain and inflammation.


WHAT’S THE DIFFERENCE BETWEEN RA AND OA?



Osteoarthritis is a deterioration of cartilage and overgrowth of bone often due to "wear and tear."

Rheumatoid arthritis is the inflammation of a Rheumatoid arthritis is the inflammation of a joint's connective tissues, such as the synovial membranes, which leads to the destruction of the joint's cartilage.


Known as the “wear-and-tear” kind of arthritisa chronic condition characterized by the breakdown of the joint’s cartilage. Cartilage is the part of the joint that cushions the ends of the bones and allows easy movement of joints. The bones and allows easy movement of joints. The breakdown of cartilage causes the bones to rub against each other, causing stiffness, pain and loss of movement in the joint.


AKA degenerative joint disease,ostoarthrosis, hypertrophic arthritis degenerative arthritis.degenerative arthritis.


stages of osteoarthritis

Cartilage loses elasticity and is more easily damaged by injury or use.Wear of cartilage causes changes to underlying bone. The bone thickens and cysts may occur under the cartilage. Bony growths, called spurs or under the cartilage. Bony growths, called spurs or osteophytes, develop near the end of the bone at the affected joint.


stages of osteoarthritis

Bits of bone or cartilage float loosely in the joint space.The joint lining, or the synovium, becomes inflamed due to cartilage breakdown causing cytokines (inflammation proteins) and enzymes cytokines (inflammation proteins) and enzymes that damage cartilage further.


The main problem in knee OA is degeneration of the articular cartilage. Articular cartilage is the smooth lining that covers smooth lining that covers the ends of bones where they meet to form the joint. The cartilage gives the knee joint freedom of movement by decreasing friction.


The articular cartilage is kept slippery by joint fluid made by the joint lining (the synovial membrane). The fluid, called synovial The fluid, called synovial fluid, is contained in a soft tissue enclosure around synovial joints called the joint capsule.


An important substance present in articular cartilage and synovial fluid is called hyaluronicacid. Hyaluronic acid acid. Hyaluronic acid helps joints collect and hold water, improving lubrication and reducing friction. It also acts by allowing cells to move and work within the joint.


When the articular cartilage degenerates, or wears away, the bone underneath is uncovered and rubs against bone. and rubs against bone. Small outgrowths called bone spurs, or osteophytes, may form in the joint.


Changes in the cartilage and bones of the joint can lead to pain, stiffness and use limitations. Deterioration of cartilage can:

Affect the shape and makeup of the joint so it doesn’t function smoothly. - limp when walk or have trouble function smoothly. - limp when walk or have trouble going up and down stairs.Cause fragments of bone and cartilage to float in joint fluid causing irritation and pain.Cause bony spurs, called osteophytes, to develop near the ends of bonesMean the joint fluid doesn’t have enough hyaluronan, which affects the joint’s ability to absorb shock.



Causes and Risk factors

there is no single known cause of osteoarthritis (OA), there are several risk factors that should be considered

AgeObesityInjury or OveruseGenetics or HeredityMuscle WeaknessOther Diseases and Types of Arthritis



Treatment

Acetaminophen Nonsteroidal anti-inflammatory drugs (NSAIDs) or COX-2 medicationsCapsaicinTramadolNarcotic pain relievers glucosamine sulfate and chondroitin sulfate


Acetaminophen

Tylenol, Anacin-3, Panadal, Phenaphen, Valadol, and others) for mild to moderate osteoarthritis. usually the first choiceusually the first choice


Nonsteroidal anti-inflammatory drugs (NSAIDs)

for moderate to severe arthritic pain.OTC NSAIDsPrescription NSAIDs include



If NSAID-induced ulcers are identified switch to alternative pain relievers.


Topical NSAIDs

$63.07


Capsaicin (Zostrix)

is an ointment prepared from the active ingredient in hot chili peppers that has been helpful for relieving painful areas in other disorders.


SALONPAS PAIN PATCH WITH CAPSAICIN


Tramadol (Ultram)

is a pain reliever that has some properties that are similar to narcotics. not as addictive, however, and may be an alternative for patients who do not respond to NSAIDs or less potent agents.



Narcotic pain relievers

oxycodone, oxymorphone, or morphinemay be necessary for severe pain that does not respond to less potent pain relievers.


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Management

Same with RA


Let’s Exercise

http://www.medicinenet.com/rheumatoid_arthritis_exercises_slideshow/article.htm



Gouty arthritis

is a disease characterized by an abnormal metabolism of uric acid, resulting in an excess of uric acid in the tissues and blood causing inflammation People with gout either produce too much uric acid, or more commonly, their bodies have a problem in removing it.AKA

goutthe disease of kingsthe king of diseases


Gouty arthritis

2 major typesPrimary Secondary


Gouty arthritis

Primary Inherited X-lined trait Caused by several inborn errors of purine metabolism

Uric acid- is the end-product of purine metabolism; excreted in urine in urine

Production of uric acid exceeds the excretion capability of kidneys Sodium urate is deposited in the synovium and other tissues which results in inflammation Males, 30’s and 40’s


Gouty arthritis

Secondary Hyperuricemia

Excessive uric acid in blood casued by anoterh disease

Affects all ages Renal insufficiency Renal insufficiency Diuretic therapyMultiple myelomaCarcinomas

Causes: decreased normal excretion of uric acid and other waste productsIncreased production of uric acid


Four Stages Of Gouty Arthritis

Asymptomatic Hyperuricemia

Acute Gout / Acute Gouty Arthritis

Interval / Intercritical

Chronic Tophaceous Gout



Asymptomatic Hyperuricemia:Asypmptomatic but with elevated blood uric acid levels

Serum uric acid level (mg/dl) Incidence of gout


Serum uric acid level (mg/dl) Incidence of gout

>9.0 7.0-8.9

7.0-8.9 0.5-0.37

<7.0 0.1%


Acute Gout / Acute Gouty Arthritishyperuricemia has caused deposits of uric acid crystals in joint spaces, leading to gouty attacks.Excruciating pain and inflammation of one or more joints – esp metatarsophalangeal joints of the great joints – esp metatarsophalangeal joints of the great toe (podagra)Increased ESR, WBC




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Interval / Intercriticalthe periods between acute gouty attacks – may be months or years after the 1st attack Asymptomatic periodNo abnormality in joints No abnormality in joints

Chronic Tophaceous Gout:the disease has caused permanent damageDeposits or urate crytals under skin and within major organs (i.e., urate kidney stone formation)


Tophi

Tophi – deposits of sodium urate crystals May occur anywhere; common in outer ear


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Dx tests

Synovial fluid analysis (shows uric acid crystals)Uric acid - bloodJoint x-rays (may be normal)Synovial biopsySynovial biopsyUric acid - urine



Management

Drug therapy Diet therapy


Management

Drug therapyacute gouty arthritis – inflammation subsides spontaneously within 3 to 5 days But if cannot tolerate pain

Colchicine (Colsalide, Novocolchicine) and NSAIDs Colchicine (Colsalide, Novocolchicine) and NSAIDs Taken for 4-7 days

(NSAIDs) -Indomethacin (Indocin), ibuprofen (Advil), and naproxen (Aleve), celecoxib (Celebrex)painkillers such as codeine, hydrocodone, and oxycodoneCorticosteroids


Management

Drug therapyChronic or repeated acute episodes

Allopurinol (Zyloprim)A xanthine oxidase inhibitor – prevents conversion of xanthineto uric acidto uric acid

Probenecid (Benemid, Benuryl)Uricosuric drug – promotes excretion of excess uric aciddrink at least 2 liters of fluid a day while taking this medication (to help prevent uric acid kidney stones from forming).

Combination drugProbenecid and Colchicine (ColBenemid)

Note: avoid aspirin – it inactivates the drug



Febuxostat (Uloric)first new medication developed specifically for the control of gout in over 40 years.Decreases formation of uric acid by the body and is a very reliable way to lower the blood uric acid level.very reliable way to lower the blood uric acid level.can be used in patients with mild to moderate kidney impairment.should not be taken with 6-mercaptopurine (6-MP), or azathioprine.


http://www.emedicinehealth.com/gout/page7_em.htm#Medications


Management

Diet therapyAvoid alcohol, anchovies, sardines, oils, herring, organ meat (liver, kidney, and sweetbreads), legumes (dried beans and peas), gravies, mushrooms, spinach, asparagus, cauliflower, consommé, and spinach, asparagus, cauliflower, consommé, and baking or brewer's yeast.


http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001459/

Limit meatAvoid fatty foods such as salad dressings, ice cream, and fried foods.Eat enough carbohydrates.Eat enough carbohydrates.If losing weight, lose it slowly. Quick weight loss may cause uric acid kidney stones to form.


http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001459/

Maria Carmela L. Domocmat, RN, MSN http://s1.hubimg.com/u/1184832_f496.jpg

Avoid all forms of aspirin and diuretics – may precipitate attackExcessive physical or emotional stress- can exacerbate disease exacerbate disease


Prevention of kidney stone formation

Increase fluid intake – prevent stone formation Dilute urine and prevent sediment formation

Alkaline ash dietCitrus fruits, juices, milk and certain dairy productsCitrus fruits, juices, milk and certain dairy productsUric acid is more soluble in high pH urine – less likely to form urinary stones


Complications

Chronic gouty arthritisKidney stonesDeposits in the kidneys, leading to chronic kidney failurekidney failure


Health & Medicine

Autoimmune disorders.RA, OA, Gout