Rheumatoid Arthritis and Gout PDF

Rheumatoid Arthritis 1 Dr. Amira Mohammed Ali Hassan Associate Professor of Medical-Surgical Nursing FON/SCU [email protected]  2 Learning objectives At the end of this lecture, the student will be able to: ❑ Explain the processes of i...

Rheumatoid Arthritis 1 Dr. Amira Mohammed Ali Hassan Associate Professor of Medical-Surgical Nursing FON/SCU [email protected]  2 Learning objectives At the end of this lecture, the student will be able to: ❑ Explain the processes of inflammation and degradation in the development of rheumatoid arthritis and gout. ❑ Identify clinical manifestations of rheumatoid arthritis and gout. ❑ Describe the assessment and diagnostic findings that may be evidenced by patients with rheumatoid arthritis and gout. ❑ Explain medical management with nursing considerations for patients with rheumatoid arthritis and gout. ❑ Discuss appropriate nursing management. 3 Rheumatoid arthritis  Rheumatoid arthritis (RA) is the one of diffuse connective tissue disease (that are chronic in nature and characterized by diffuse inflammation and degeneration in the connective tissues)  RA is commonly used as the prototype for inflammatory arthritis.  Rheumatoid arthritis (RA) is a chronic systemic inflammatory disorder characterized by potentially deforming polyarthritis and a wide spectrum of extra-articular manifestations  Epidemiology 4 The prevalence of RA is estimated to be 1% worldwide Occurring nearly twice as often in women as in men The onset of RA typically occurs between the third and fourth decades of life Genetics contribute to 50% or 60% of the risk of developing RA 5 Epidemiology  Estrogen is known to stimulate the immune system; pregnant patients often experience a remission of RA symptoms, and women who take oral contraceptives appear to be protected somewhat against the development of RA  Diets rich in fish, olive oil, and other omega-3 fatty acid sources are associated with a lower risk of developing RA  Deficiency of vitamin D is associated with RA  Cigarette smoking: increases RA risk  6 Pathophysiology  RA-induced joint destruction begins with inflammation of the synovial lining that surrounds the joint space  This normally thin membrane proliferates and transforms into the synovial pannus  The pannus, a highly erosive enzyme-laden inflammatory exudate, invades articular cartilage (leading to narrowing of joint spaces), erodes bone (resulting in osteoporosis), and destroys periarticular structures (ligaments, tendons), resulting in joint deformities 7 Pathophysiology 8  Clinical presentation 9  Insidious onset  Slow development of sign & symptoms  Early nonspecific symptoms such as fatigue, malaise, diffuse musculoskeletal pain  Patients usually experience prolonged morning stiffness (more specific symptoms) on awakening, which usually lasts 30 to 60 minutes but can be present all day with decreasing intensity after arising  Duration of morning stiffness also can be a useful marker of disease activity  Bilaterally symmetrical joint swelling and pain, involving the MCP and PIP joints of the hands and MTP joints of the feet  Decreased range of motion (ROM), and sometimes muscle atrophy around affected joints 10 11 12 Clinical presentation  Joint pain, swelling, warmth, erythema, and lack of function.  Palpation of the joints reveals spongy or boggy tissue.  The pattern of joint involvement begins with the small joints in the hands, wrists, and feet.  As the disease progresses, the knees, shoulders, hips, elbows, ankles, cervical spine, and temporomandibular joints are involved.  Joints that are hot, swollen, and painful are not easily moved.  The patient tends to guard or protect these joints through immobilization.  Immobilization for extended periods can lead to contractures, creating soft tissue deformity.  Deformities of the hands and feet are common 13 Clinical presentation  RA is a systemic disease, which is reflected by the extra- articular manifestations that can accompany joint involvement  Organ system involvement may be extensive. Pleuropulmonary manifestations (e.g., pleuritis, development of pulmonary nodules, interstitial fibrosis, pneumonitis, and rarely arteritis of the pulmonary vasculature) also can accompany the articular involvement of RA  Cardiac involvement can present as pericarditis or myocarditis  Vasculitis, another extra-articular manifestation of RA, can involve any organ system and can vary in seriousness from mild to potentially life-threatening 14 Clinical presentation  Some extra-articular manifestations occur as syndromes  Sjogren syndrome includes dry eyes (keratoconjunctivitis sicca),dry mouth (xerostomia), and connective tissue disease  Felty syndrome is characterized by chronic arthritis, splenomegaly, and neutropenia; thrombocytopenia, anemia, and lymphadenopathy also may be present 15 Advanced rheumatoid arthritis:  The deformity may be caused by misalignment resulting from swelling, progressive joint destruction, or the subluxation (partial dislocation) that occurs when a bone slips over another and eliminates the joint space.  RA is a systemic disease with multiple extra-articular features. Most common are fever, weight loss, fatigue, anemia, lymph node enlargement, and Raynaud’s phenomenon (cold- andstress-induced vasospasm causing episodes of digital blanching or cyanosis).  The four stages of rheumatoid 16 arthritis (RA)  Stage 1, or early RA: The inflammation of the synovium (the lining of the joints) begins, but there is no joint damage yet. Symptoms may not appear at this stage.  Stage 2, or moderate RA: The inflammation of the synovium spreads and causes cartilage damage and joint erosion. Symptoms such as pain, swelling, stiffness, and reduced mobility may appear.  Stage 3, or severe RA: The inflammation and damage of the synovium, cartilage, and bones continue and affect the shape and alignment of the joints. Symptoms such as deformity, disability, and loss of function may occur.  Stage 4, or end stage RA: The inflammation of the synovium stops, but the joint damage is irreversible and may lead to joint fusion. Symptoms such as chronic pain and immobility may persist. Criteria for Diagnosis of Rheumatoid Arthritis 17  Diagnosis of RA is based on joint involvement, serology, acute- phase reactants, and symptom duration 18 Assessment & Diagnostic Finding  The history and physical examination address manifestations such as bilateral and symmetric stiffness, tenderness, swelling, and temperature changes in the joints.  The patient is also assessed for extra-articular changes; these often include weight loss, sensory changes, lymph node enlargement, and fatigue.  Rheumatoid factor (are autoantibodies associated with rheumatoid arthritis) is present in more than 80% of patients with RA 19 Assessment & Diagnostic Finding  The erythrocyte sedimentation rate (ESR) is significantly elevated with RA.  C-reactive protein and antinuclear antibody test results may also be positive.  The red blood cell count and C4 complement component are decreased  Arthrocentesis: shows synovial fluid that is cloudy, milky, or dark yellow and contains numerous inflammatory components, such as leukocytes and complement.  X-ray studies: show characteristicbony erosions and narrowed joint spaces occurring later in the disease.  Treatment 20  The treatment of RA involves a combination of interventions, which include rest, exercise (physical therapy), emotional support, occupational therapy, and drugs  Specific treatment should be individualized based on joint function, degree of disease activity, patient age, sex, occupation, family responsibilities, drug costs, and results of previous therapy  The ultimate goal of RA treatment is disease remission; however, because sustained remission is uncommon, minimizing disease activity to provide pain relief, help patients maintain activities of daily living, maximize their quality of life, and slow joint damage is also a goal  Nonpharmacologic Pain Management 21  Heat applications are helpful in relieving pain, stiffness, and muscle spasm.  Superficial heat may be applied in the form of warm tub baths or showers and warm moist compresses.  Paraffin baths (dips), which offer concentrated heat, are helpful to patients with wrist and small-joint involvement.  Maximum benefit is achieved within 20 minutes after application.  More frequent use for shorter lengths of time is most beneficial.  Therapeutic exercises can be carried out more comfortably and effectively after heat has been applied.  Nonpharmacologic Pain Management 22  Therapeutic exercises can be carried out more comfortably and effectively after heat has been applied.  Devices such as braces, splints, and assistive devices for ambulation (e.g., canes, crutches, walkers) ease pain by limiting movement or stress from putting weight on painful joints.  Acutely inflamed joints can be rested by applying splints to limit motion.  Canes and crutches can relieve stress from inflamed and  painful weight-bearing joints while promoting safe ambulation.  Cervical collars may be used to support the weight of the head and limit cervical motion. 23 Treatment  In early-stage RA:  Treatment begins with education, a balance of rest and exercise.  Although symptoms of RA generally can be controlled by conservative management, more aggressive therapy is needed to prevent disease progression and disability  Although NSAIDs provide rapid anti-inflammatory and analgesic effects, they do not prevent or slow joint destruction  Therefore, Disease-modifying antirheumatic drugs (DMARD) therapy should be initiated for all patients diagnosed with RA  Treatment 24 Traditional DMARDs have demonstrated the ability to slow disease progression include:  Hydroxychloroquine [HCQ]  Sulfasalazine [SSZ]  Methotrexate [MTX],  Leflunomide [LEF]  Minocycline [MIN]  Gold  Azathioprine [AZA]  D-penicillamine  D-penicillamine is seldom used because of a very slow onset of action and numerous side effects  These agents, alone or in combination, should be considered as initial therapy for most patients  Treatment 25  The newest class of DMARDs is the biologic agents include  TNF-α inhibitors (infliximab, etanercept, adalimumab, certolizumab pegol [CZP],and golimumab[GLM]),  IL-1 receptor antagonist (anakinra)  Anti-B cell therapy (rituximab [RXB])  IL-6 receptor antagonist (tocilizumab[TZB])  T-cell modulator (abatacept)  Despite recent advances in RA treatment, MTX remains the initial treatment of choice for most patients with RA owing to its strong efficacy and favorable safety profile  TNF-α agents are recommended for patients who fail to achieve an adequate response either with MTX alone or MTX in combination with other traditional DMARDs, or for patient's intolerant to MTX 26 Treatment  Corticosteroids are also potent anti-inflammatory agents that slow the progression of joint damage in RA  they are reserved for brief periods of active disease (low-dose oral therapy), or for isolated joints experiencing disease flares (local intraarticular injection) because of serious adverse effects associated with long-term systemic use 27 In moderate &erosive stage:  A formal program with occupational and physical therapy is prescribed to educate the patient about principles of joint protection, pacing activities, work simplification, range of motion, and muscle-strengthening exercises.  The patient is encouraged to participate actively in the management program.  Cyclosporine (an immunomodulator, may be added to enhance the disease modifying effect of methotrexate).  In Persistent erosive RA 28  Reconstructive surgery and corticosteroids are often used.  Reconstructive surgery is indicated when pain cannot be relieved by conservative measures.  Surgical procedures include synovectomy (excision of the synovial membrane), tenorrhaphy (suturing a tendon), arthrodesis (surgical fusion of the joint), and arthroplasty (surgical repair and replacement of the joint).  In Advanced & Unremitting RA 29  Immunosuppressive agents are prescribed because of their ability to affect the production of antibodies at the cellular level.  These include high-dose methotrexate (Rheumatrex), cyclophosphamide (Cytoxan), and azathioprine (Imuran).  These medications, however, are highly toxic and can produce bone marrow suppression, anemia, gastrointestinal disturbances, and rashes.  Anti-depressant agent (treatment of depression & sleep deprivation)  For more severe and longstanding cases of RA who have failed to respond to or are intolerant of disease-modifying antirheumatic drugs. The device, a protein A Immunoadsorption column (Prosorba), is used in 12 weekly 2-hour apheresis treatments to bind IgG 30 Nutritional therapy  A dietary history identifies usual eating habits and food preferences.  Food selection should include the daily requirements from the basic food groups, with emphasis on foods high in vitamins, protein, and iron for tissue building and repair.  For the extremely anorexic patient, small, frequent feedings with increased protein supplements may be prescribed.  Some medications (ie, oral corticosteroids) used in RA treatment stimulate the appetite and, when combined with decreased activity, may lead to weight gain  Patients may need to be counseled about eating a healthy, calorie- restricted diet.  Nursing Assessment 31  The assessment of a patient with RA can contribute to its diagnosis.  History and physical exam. The history and physical examination address manifestations such as bilateral and symmetric stiffness, tenderness, swelling, and temperature changes in the joints.  Extra-articular changes. The patient is also assessed for extra-articular changes, and these include weight loss, sensory changes, lymph node enlargement, and fatigue. 32 Nursing Diagnosis Acute and chronic pain related to inflammation and increased disease activity, tissue damage, fatigue, or lowered tolerance level. Fatigue related to increased disease activity, pain, inadequate sleep/rest, deconditioning, inadequate nutrition, and emotional stress/depression Impaired physical mobility related to decreased range of motion, muscle weakness, pain on movement, limited endurance, lack or improper use of ambulatory devices. Self-care deficit related to contractures, fatigue, or loss of motion. Disturbed body image related to physical and psychological changes and dependency imposed by chronic illness. Ineffective coping related to actual or perceived lifestyle or role changes. 33 The major goals for a patient with RA are Improvement in comfort level. Incorporation of pain management techniques into daily life. Incorporation of strategies necessary to modify fatigue as part of the daily activities. Attain and maintain optimal functional mobility. Adapt to physical and psychological changes imposed by the rheumatic disease. Use of effective coping behaviors for dealing with actual or perceived limitations and role changes.  Nursing intervention of Relieving Pain and 34 Discomfort Provide a variety of comfort measures (eg, application of heat or cold; massage, position changes, rest; foam mattress, supportive pillow, splints; relaxation techniques, diversional activities). Administer anti-inflammatory, analgesic, and slow- acting antirheumatic medications as prescribed. Individualize medication schedule to meet patient’s need for pain management. Encourage verbalization of feelings about pain and chronicity of disease. Teach pathophysiology of pain and rheumatic disease and assist patient to recognize that pain often leads to unproven treatment methods. Assist in identification of pain that leads to use of unproven methods of treatment. Assess for subjective changes in pain. 35 Nursing intervention of Reducing Fatigue Provide instruction about fatigue: Describe relationship of disease activity to fatigue; describe comfort measures while providing them; Develop and encourage a sleep routine (warm bath and relaxation techniques that promote sleep); Explain importance of rest for relieving systematic, articular, and emotional stress. Explain how to use energy conservation techniques (pacing, delegating, setting priorities). Identify physical and emotional factors that can cause fatigue. Facilitate development of appropriate activity/rest schedule. Encourage adherence to the treatment program. Refer to and encourage a conditioning program. Encourage adequate nutrition, including source of iron from food and supplements.  Nursing intervention of Increasing Mobility 36 Encourage verbalization regarding limitations in mobility. Assess need for occupational or physical therapy consultation: Emphasize range of motion of affected joints; Promote use of assistive ambulatory devices; Explain use of safe footwear; Use individual appropriate positioning/posture. Assist to identify environmental barriers. Encourage independence in mobility and assist as needed: Allow ample time for activity; Provide rest period after activity; reinforce principles of joint protection and work simplification. Initiate referral to community health agency  Facilitating Self Care 37 Assist patient to identify self-care deficits and factors that interfere with ability to perform self- care activities. Develop a plan based on the patient’s perceptions and priorities on how to establish and achieve goals to meet self-care needs, incorporating joint protection, energy conservation, and work simplification concepts: Provide appropriate assistive devices; reinforce correct and safe use of assistive devices; allow patient to control timing of self-care activities; explore with the patient different ways to perform difficult tasks or ways to enlist the help of someone else.  Nursing intervention of Improving Body 38 Image and Coping Skills Help patient identify elements of control over disease symptoms and treatment. Encourage patient’s verbalization of feelings, perceptions, and fears. Identify areas of life affected by disease. Answer questions and dispel possible myths. Develop plan for managing symptoms and enlisting support of family and friends to promote daily function.  Monitoring and Managing Potential 39 Complications Help patient recognize and deal with side effects from medications. Monitor for medication side effects, including GI tract bleeding or irritation, bone marrow suppression, kidney or liver toxicity, increased incidence of infection, mouth sores, rashes, and changes in vision. Other signs and symptoms include bruising, breathing problems, dizziness, jaundice, dark urine, black or bloody stools, diarrhea, nausea and vomiting, and headaches. Monitor closely for systemic and local infections, which often can be masked by high doses of corticosteroids  Gout 40 41 Gout Definition: is a heterogeneous group of conditions related to a genetic defect of purine metabolism resulting in hyperuricemia. Over secretion of uric acid or a renal defect resulting in decreased excretion of uric acid, or a combination of both, occurs.  Gout 42  Gout is a disease that most commonly manifests as recurrent episodes of acute joint pain and inflammation secondary to the deposition of monosodium urate (MSU) crystals in the synovial fluid and lining  MSU deposition in the urinary tract can cause urolithiasis and urinary obstruction  Patients with gout cycle between flares of acute joint pain and inflammation and inter-critical gout (i.e., periods of quiescence with no symptoms of the disease)  They can also exhibit chronic tophaceous gout and hyperuricemia 43 Epidemiology  It occurs more commonly in males than females.  Men are three to four times more likely to be diagnosed with gout than women.  The incidence of gout increases with age, body mass index, alcohol consumption, hypertension, and diuretic use  Evidence links the consumption of fructose-rich beverages with the risk of gout for both men and women  Types 44 Primary Hyperuricemia In primary hyperuricemia, elevated serum urate levels or manifestations of urate deposition appear to be consequences of faulty uric acid metabolism. Primary hyperuricemia may be due to severe dieting or starvation, excessive intake of foods that are high in purines (shellfish, organ meats), or heredity. 45 Types Secondary Hyperuricemia In secondary hyperuricemia, gout is a clinical feature secondary to any of a number of genetic or acquired processes, including conditions in which there is an increase in cell turnover (leukemia, multiple myeloma, some types of anemia, psoriasis) and an increase in cell breakdown. Altered renal tubular function, either as a major action or as an unintended side effect of certain pharmacologic agents (diuretics such as thiazides and furosemide), low-dose salicylates, and ethanol can contribute to uric acid underexcretion. 46 Risk factors  HTN  Diabetes  Hyperlipidemia  Obesity  CHD  Although this relationship is strong, causality is controversial  Renal dysfunction  Ethanol consumption  Overindulgence of alcohol has been linked to acute gout attacks 47 Pathophysiology of gout Hyperuricemia (serum concentration greater than 7 mg/dL [0.4 fmol/L]) can but does not always cause monosodium urate crystal deposition. However, as uric acid levels rise, risk increases. Attacks of gout appear to be related to sudden increases or decreases of serum uric acid levels. When the urate crystals precipitate within a joint, an inflammatory response occurs, and an attack of gout begins. With repeated attacks, accumulations of sodium urate crystals, called tophi, are deposited in peripheral areas of the body, such as the great toe, the hands, and the ear. 48 Pathophysiology of gout Renal urate lithiasis (kidney stones) with chronic renal disease secondary to urate deposition may develop. The finding of urate crystals in the synovial fluid of asymptomatic joints suggests that factors other than crystals may be related to the inflammatory reaction. Recovered monosodium urate crystals are coated with immunoglobulins that are mainly immunoglobulin G (IgG). IgG enhances crystal phagocytosis, thereby demonstrating immunologic activity. 49 50 Clinical Manifestations  Acute gouty arthritis (recurrent attacks of severe articular and periarticular inflammation), tophi (crystalline deposits accumulating in articular tissue, osseous tissue, soft tissue, and cartilage).  Gouty nephropathy (renal impairment), and uric acid urinary calculi.  For hyperuricemic people who are going to develop gout, acute arthritis is the most common early clinical manifestation. The metatarsophalangeal joint of the big toe is the most commonly affected (75% of patients). 51 Clinical Manifestations  The abrupt onset often occurs at night, awakening the patient with severe pain, redness, swelling, and warmth of the affected joint.  Early attacks tend to subside spontaneously over 3 to 10 days  even without treatment.  The attack is followed by a symptom-free period (the intercritical stage) until the next attack, which may not come for months or years.  Uric acid deposits may cause renal stones and kidney damage.  HYPERURICEMIA 52 Chronic Gout Drug therapy to lower SUA concentrations is warranted for patients who have recurrent gout attacks (at least two attacks per year), arthropathy, tophi, or radiographic changes related to gout GOAL OF URATE-LOWERING THERAPY The SUA concentration in a patient who has clinical gout should be decreased to 6 mg/dL or less The BSR/BHPR guidelines state a goal of less than 5 mg/dL based on expert opinion  Treatment of Acute Gout 53 GOALS OF THERAPY  The primary goal in the treatment of an acute attack of gout for is to relieve pain and inflammation  The immediate goal of therapy should not be aimed at decreasing the SUA concentration with ULT such as allopurinol, febuxostat, or probenecid  Patients most likely have been hyperuricemic for several months or years, and it is not necessary to treat the hyperuricemia immediately  Acute gouty arthritis can be effectively treated in most instances by a nonsteroidal antiinflammatory drug (NSAID), colchicine, or corticosteroids 54 Medical Management  Colchicine (oral or parenteral) or an NSAID such as indomethacin is used to relieve an acute attack of gout.  Uricosuric agents, such as probenecid, correct hyperuricemia and dissolve deposited urate.  Allopurinol is also effective, but its use is limited because of the risk for toxicity.  When the patient has, or is at risk for, renal insufficiency or renal calculi (kidney stones), allopurinol is the medication of choice. 55 Nursing Management Patients should be encouraged to restrict consumption of foods high in purines, especially organ meats, and to limit alcohol intake. Maintenance of normal body weight should be encouraged. In an acute episode of gouty arthritis, pain management is essential. During the intercritical period, the patient feels well and may abandon preventive behaviors, which may result in an acute attack. Acute attacks are most effectively treated if therapy is begun early in the course. 56 57