REPUBLIC OF THE PHILIPPINES

Mariano Marcos State University

COLLEGE OF HEALTH SCIENCES Department of Nursing Batac City

SYSTEMIC LUPUS ERYTHEMATOSUS

Prepared by: Agcaoili, KristelAngelie Agullana, DharlineAbbygale Alog, John Alwin Aragon, Jesusa Mae Ballesteros, Gerly Bolusan, Kelvin Bonoan, Rodalie Cabrera, GuiaAmerie Caliw-caliw, Hannah Lou Cario, Mary Joy BSN III-B (Group 1)

Presented to: Mrs. Cherryl M. sacro C.I.

June 30, 2011

Systemic Lupus Erythematosus I. Introduction A. Etymology There are several explanations ventured for the term lupus erythematosus. Lupus is Latin for wolf and "erythro" is derived from , Greek for "red." All explanations originate with the reddish, butterfly-shaped malar rash that the disease classically exhibits across the nose and cheeks. Some doctors thought the rash resembled the pattern of fur on a wolf's face.In other accounts, doctors thought that the rash, which was often more severe in earlier centuries, created lesions that resembled wolf bites or scratches.Another account claims that the term "lupus" did not come from Latin directly, but from the term for a French style of mask that women reportedly wore to conceal the rash on their faces. The mask is called a "loup," French for "wolf." B. Definition Systemic lupus erythematosus (SLE), or lupus, is an autoimmune disease in which a person's immune system attacks various organs or cells of the body, causing damage and dysfunction. Lupus is called a multisystem disease because it can affect many different tissues and organs in the body. It is a Type III hypersensitivity reaction caused by antibody-immune complex formation. II. Incidence and Prevalence of Lupus In the general population, SLE affects approximately 1 in 2000 individuals. Lupus is most common in women of childbearing age, but it can occur in men and women of any age. Approximately 90% of patients with systemic lupus erythematosus are women. SLE occurs about 3 times more often in African-American women than Caucasian women and the condition is also more common in Hispanic, Asian, and Native American women. An underlying hormonal change may explain why the disease affects so many more women. Genetic factors may also be involved. Familial aggregation occurs in 10% of people having a first-degree relative with SLE, including its occurrence in identical twins. III. Risk Factors Sex. Lupus is more common in women. Age. Although lupus affects people of all ages, including infants, children and older adults, it's most often diagnosed between the ages of 15 and 40. Race. Lupus is more common in blacks, Hispanics and Asians. Sunlight. Exposure to the sun may bring on lupus skin lesions or trigger an internal response in susceptible people. Certain prescription medications. Drug-induced lupus results from the long-term use of certain prescription drugs. Although many medications can potentially trigger lupus, examples of drugs most clearly linked with the disease include the antipsychotic chlorpromazine; high blood pressure medications, such as hydralazine (Apresoline); the tuberculosis drug isoniazid and the heart medication procainamide (Pronestyl, Procanbid), among others. It usually takes several months or years of therapy with these drugs before symptoms appear, and even then, only a small percentage of people will ever develop lupus. Infection with Epstein-Barr virus. Almost everyone has been infected with a common human virus called Epstein-Barr virus. Epstein-Barr virus causes nonspecific signs and symptoms, such as fever and sore throat. Once the initial infection subsides, the virus remains dormant in the cells of your immune system unless something reactivates the virus. For reasons that aren't clear, recurrent Epstein-Barr infections seem to increase the risk of developing lupus.

Exposure to chemicals. It's difficult to prove that chemicals can cause or increase the risk of a disease. But some studies have shown that people who work in jobs that involve exposure to mercury and silica may have an increased risk of lupus. Smoking cigarettes also may increase your risk of developing lupus. IV. Pathophysiology People with SLE produce several autoantibodies. The primary autoantibodies produced are directed at the cell nuclei and are called antinuclear antibodies (ANA's). SLE produces autoantibodies against double-stranded DNA, and the presence of these antibodies in the serum is considered typical off SLE. Normally, the T suppressor cells prevent autoantibody formation. In SLE, a defect in the T suppressor cell prevents this protective process. Natural killer (NK) cell function is also suppressed; NK cells cannot kill abnormal cells as readily. There are inherited defects in complement factors and cell surface receptors that normally assist with clearing immune complexes. ANA's do not cause much of cellular destruction alone, primarily because ANA's do not come in contact with intact cell nuclei. When cells die, the nuclei are released and then bind to the ANA's. The immune complex that is formed triggers the inflammatory response, which is the primary cause of tissue damage. In addition, the immune complex is large and is often deposited in tissue. Deposition of this complex causes even more tissue damage by initiating the complement cascade and further increasing inflammation. A common site of deposition is the basement membrane of the kidney, which leads to glomerulonephritis. The complexes can also cause vasculitis, or inflammation of the vessels, resulting in a decrease of oxygen in organs and tissues. The immune complexes can also be deposited in the heart and brain. V. The 1982 Revised Criteria for the Diagnosis of Systemic Lupus Erythematosus (SLE) o The diagnosis of SLE is confirmed if a client has any 4 of the 11 criteria present, either serially or simultaneously, during any observation period. Criterion 1. Malar rash 2. Discoid rash 3. Photosensitivity 4. Oral ulcers 5. Arthritis 6. Serositis 7. Renal disorder 8. Neurologic disorder 9. Hematologic disorder 10. Immunologic disorder 11. Antinuclear antibody Diagnostic procedures Antinuclear antibody (ANA) testing and anti-extractable nuclear antigen (anti-ENA) form the mainstay of serologic testing for SLE. Several techniques are used to detect ANAs. Clinically the most widely used method is indirect immunofluorescence. The pattern of fluorescence suggests the type of antibody present in the patient's serum. ANA screening yields positive results in many connective tissue disorders and other autoimmune diseases, and may occur in normal individuals. Subtypes of antinuclear antibodies include anti-

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Smith and anti-double stranded DNA (dsDNA) antibodies (which are linked to SLE) and anti-histone antibodies (which are linked to drug-induced lupus). Anti-dsDNA antibodies are highly specific for SLE; they are present in 70% of cases, whereas they appear in only 0.5% of people without SLE. The antidsDNA antibody titers also tend to reflect disease activity, although not in all cases. Other ANA that may occur in SLE sufferers areanti-U1 RNP (which also appears in systemic sclerosis), SS-A (or anti-Ro) and SS-B (or anti-La; both of which are more common in Sjgren's syndrome). SS-A and SS-B confer a specific risk for heart conduction block in neonatal lupus. Other tests routinely performed in suspected SLE are complement system levels (low levels suggest consumption by the immune system), electrolytes and renal function (disturbed if the kidney is involved), liver enzymes, and complete blood count. VII. Medical Management 1. NSAIDs 2. Antimalarials 3. Corticosteroids 4. Immunosuppressives VIII. NURSING MANAGEMENT OF THE MEDICAL CLIENT 1. Nursing Intervention for client with SLE depends on how the client responds to the condition and on the severity and specific types of clinical manifestations. 2. In a newly diagnosed client, you can expect knowledge deficits with respect to the diagnosis itself, prescribed drug therapies and the prognosis. 3. Explain how to relieve anxiety and avoid misunderstandings. This is particularly important in terms of the prescribed medications. 4. Advise the client and significant others of the action, side effects, and potential interactions of prescribed medications, especially corticosteroids. 5. During follow-up visits, review changes in all body systems. 6. Do the physical examination is needed, with attention given to skin, muscles and joints. 7. CNS involvement is common, and a complete psychosocial assessment is important to detect changes in cognition and emotional stability. 8. During exacerbations, provide physiologic support to prevent skin breakdown, maintain nutritional and metabolic status and minimize the risk of opportunistic infection. 9. Also, provide emotional support to the client facing a chronic, potentially fatal disease. Clients may experience grief reaction following diagnosis, with exacerbations, or both. Allow for verbalization of these feelings. In such situations, be supportive and understanding; when necessary, refer the client or family members for counseling. NURSING DIAGNOSES AND POSSIBLE INTERVENTIONS Nursing Diagnosis #1 Fatigue related to chronic inflammation and altered immunity as manifested by lack of energy and inability to maintain usual routine. INTERVENTIONS RATIONALE 1. Determine patient s physical To plan daily activities limitations 2. Assist patient in assigning priority to To accommodate energy level activities

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3. Assist patient to schedule rest periods 4. Teach activity organization and timemanagement techniques 5. Encourage alternate rest and activity periods 6. Instruct the patient and significant others to notify health care provider if signs and symptoms of fatigue persist

To temporarily minimize the effects of fatigue To prevent fatigue To promote recuperation and to foster maximum participation in activities To increase patient s support and family s understanding of disease and related problems

Nursing Diagnosis # 2 Acute pain related to inflammatory processes and inadequate comfort measures as manifested by complaints of joint pain, lack of relief from pain- relieving measures, reduction of activities to avoid exacerbating pain. INTERVENTIONS 1. Perform a comprehensive assessment of pain to include location, characteristics, onset/ duration, frequency, quality, intensity or severity of pain and precipitating factors 2. Teach use of nonpharmacologic techniques to alleviate pain such as relaxation and guided imagery 3. Instruct the patient to avoid stressful activities 4. Instruct the patient to do diversional activities such as reading books RATIONALE To plan appropriate interventions

To replace or supplement analgesics

To avoid the occurrence of pain So that the patient will not focus to the occurrence of pain and will likely make the patient be relaxed