Systemic Lupus Erythematosus PDF

11/21/23, 3:15 PM Realizeit for Student Systemic Lupus Erythematosus SLE is an inflammatory, autoimmune disorder that affects nearly every organ in the body. The overall incidence of SLE is estimated to be 1.8 to 7.6 per 100,000 people (Centers for Disease Control and Prevention [CDC], 2018). It o...

11/21/23, 3:15 PM Realizeit for Student Systemic Lupus Erythematosus SLE is an inflammatory, autoimmune disorder that affects nearly every organ in the body. The overall incidence of SLE is estimated to be 1.8 to 7.6 per 100,000 people (Centers for Disease Control and Prevention [CDC], 2018). It occurs 4 to 12 times more frequently in women than in men and occurs more often in African Americans, Hispanics/Latino Americans, Asians, and American Indians/Alaska Natives than among White Americans (CDC, 2018). In addition to SLE, other forms of adult lupus exist, including subacute cutaneous or discoid lupus erythematous, and drug-induced lupus (Aringer, Costenbader, Daikh, et al., 2019). Pathophysiology While the exact cause is not known, SLE starts with the body’s immune system inaccurately recognizing one or more components of the cell’s nucleus as foreign, seeing it as an antigen. The immune system starts to develop antibodies to the nuclear antigen. In particular, B cells begin to overproduce antibodies with the help of multiple cytokines such as B-lymphocyte stimulator (BLyS), which is overexpressed in SLE. The antibodies and antigens form antigen–antibody complexes and have the propensity to get trapped in the capillaries of visceral structures. The antibodies also act to destroy host cells. It is thought that those two mechanisms are responsible for the majority of the clinical manifestations of this disease process. The immunoregulatory disturbance is thought to be brought about by some combination of four distinct factors: genetic, immunologic, hormonal, and environmental (Norris, 2019). Research into the genetic origins of SLE has thus far revealed that multiple genes are likely implicated in the development of SLE (Norris, 2019). The large majority of SLE cases, however, remain sporadic and unrelated to family medical history. Given the high number of women with SLE compared with men, it is hypothesized that female sex hormones (estrogen) play a role in the predisposition to SLE. Estrogen may contribute to the body’s response of overreacting to the body’s own tissues. Although genetics and hormones likely play a role in the predisposition of SLE, it is hypothesized that exogenous or environmental triggers are also implicated in the onset of the disease process. These triggers may include cigarette smoke, ultraviolet rays, exposure from sunlight and fluorescent light bulbs, medications (hydralazine, minocyline, or procainamide), viral infections, emotional stress, stress on the body (e.g., surgery, pregnancy), and silica dust exposure in the occupational setting (Norris, 2019). Clinical Manifestations https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IX01cMmy1tXd%2bA0lN30h55hoLMwB%2fCluMLMNMH… 1/5 11/21/23, 3:15 PM Realizeit for Student SLE is an autoimmune, systemic disease that can affect any body system (Fig. 34-2). The disease process involves chronic states where symptoms are minimal or absent and acute flares where symptoms and lab results are elevated. Symptoms most often include fever, fatigue, skin rashes, as well as joint pain and swelling (Aringer et al., 2019; CDC, 2018). The mucocutaneous, musculoskeletal, renal, nervous, cardiovascular, and respiratory systems are most commonly involved. Less commonly affected are the gastrointestinal tract and liver as well as the ocular system. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IX01cMmy1tXd%2bA0lN30h55hoLMwB%2fCluMLMNMH… 2/5 11/21/23, 3:15 PM Realizeit for Student https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IX01cMmy1tXd%2bA0lN30h55hoLMwB%2fCluMLMNMH… 3/5 11/21/23, 3:15 PM Realizeit for Student Figure 34-2 Clinical manifestations of SLE. Reprinted with permission from Norris, T. L. (2019). Porth’s pathophysiology: Concepts of altered health states (10th ed., Fig. 50.5). Philadelphia, PA: Wolters Kluwer. Some type of cutaneous system manifestation is experienced in up to 85% of patients with SLE (Norris, 2019). Several skin manifestations may occur in patients with SLE, including subacute cutaneous lupus erythematosus, which involves papulosquamous or annular polycyclic lesions, and a discoid rash, which is a chronic rash with erythematous papules or plaques and scaling and can cause scarring and pigmentation changes (Aringer et al., 2019). In some cases, the only skin involvement may be a discoid rash. In some patients with SLE, the initial skin involvement is the precursor to more systemic involvement. The lesions often worsen during exacerbations (flares) of the systemic disease and possibly are provoked by sunlight or artificial ultraviolet light (Norris, 2019). Oral ulcers, which may accompany skin lesions, may involve the buccal mucosa or the hard palate, occur in crops, and are often associated with exacerbations. Other cutaneous manifestations include splinter hemorrhages, alopecia, and Raynaud’s phenomenon. Joint pain and swelling occur in more than 90% of patients with SLE (Norris, 2019). Joint swelling, tenderness, and pain on movement are also common. Frequently, these are accompanied by morning stiffness. The cardiac system is also commonly affected in SLE. Pericarditis is the most common cardiac manifestation (Norris, 2019). Patients may present with substernal chest pain that is aggravated by movement or inspiration. Symptoms can be acute and severe or last for weeks at a time. Other cardiac symptoms may involve myocarditis, hypertension, cardiac arrhythmias, and valvular incompetence. Nephritis as a result of SLE, also referred to as lupus nephritis, occurs due to a buildup of antibodies and immune complexes that cause damage to the nephrons. Serum creatinine levels and urinalysis are used in screening for renal involvement. Early detection allows for prompt treatment so that renal https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IX01cMmy1tXd%2bA0lN30h55hoLMwB%2fCluMLMNMH… 4/5 11/21/23, 3:15 PM Realizeit for Student damage can be prevented. Renal involvement may lead to hypertension, which also requires careful monitoring and management. Central nervous system involvement is widespread, encompassing the entire range of neurologic disease. The varied and frequent neuropsychiatric presentations of SLE are now widely recognized and include psychosis, cognitive impairment, seizures, peripheral and cranial neuropathies, transverse myelitis, and strokes. These are generally demonstrated by subtle changes in behavior patterns or cognitive ability. Assessment and Diagnostic Findings Diagnosis of SLE is based on a complete history, physical examination, and blood tests. In addition to the general assessment performed for any patient with a rheumatic disease, assessment for known or suspected SLE has special features. The skin is inspected for erythematous rashes. Cutaneous erythematous plaques with an adherent scale may be observed on the scalp, face, or neck. Areas of hyperpigmentation or depigmentation may be noted, depending on the phase and type of disease. The patient should be questioned about skin changes (because these may be transitory) and specifically about sensitivity to sunlight or artificial ultraviolet light. The scalp should be inspected for alopecia and the mouth and throat for ulcerations reflecting gastrointestinal involvement. Cardiovascular assessment includes auscultation for pericardial friction rub, possibly associated with myocarditis and accompanying pleural effusions. The pleural effusions and infiltrations, which reflect respiratory insufficiency, are demonstrated by abnormal lung sounds. Papular, erythematous, and purpuric lesions developing on the fingertips, elbows, toes, and extensor surfaces of the forearms or lateral sides of the hand that may become necrotic suggest vascular involvement. Joint swelling, tenderness, warmth, pain on movement, stiffness, and edema may be detected on physical examination. The joint involvement is often symmetric and similar to that found in RA. The neurologic assessment is directed at identifying and describing any central nervous system changes. The patient and family members are asked about any behavioral changes, including manifestations of neurosis or psychosis. Signs of depression are noted, as are reports of seizures, chorea, or other central nervous system manifestations. The antinuclear antibody (ANA) is positive in more than 95% of patients with SLE, indicating exceptional specificity (Aringer et al., 2019). Other laboratory tests include anti-DNA (antibody that develops against the patient’s own DNA), anti-ds DNA (antibody against DNA that is highly specific to SLE, which helps differentiate it from drug-induced lupus), and anti-Sm (antibody against Sm, which is a specific protein found in the nucleus). Other blood work includes the CBC, which may reveal anemia, thrombocytopenia, leukocytosis, or leukopenia. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IX01cMmy1tXd%2bA0lN30h55hoLMwB%2fCluMLMNMH… 5/5