Systemic Lupus Erythematosus Test Questions Essay Example

hormonal, genetic, and environmental factors such as thermal burns and sunlight. Additionally, certain medications including procainamide, apresoline, isoniazid, antiseizures, and chlorpromazine have been linked to drug-induced SLE. The overproduction of autoantibodies is attributed to abnormal function of suppressor T-cells, which results in tissue damage and deposition of immune complexes. Inflammation also triggers the production of antigens, further fueling the antibody cycle.

SLE can go undiagnosed for a few years as the onset can be acute or insidious, affecting multiple body systems. The disease spreads throughout the body via the circulatory system (Smeltzer ; Bare, 2003). Inflammatory processes impact the integumentary system, resulting in plaques with scaling that can cause scarring and pigmentation changes, chronic rash with erythematous papules, or papulosquamous or annular polycyclic lesions (subacute cutaneous lupus erythematosus) (Smeltzer ; Bare, 2003). The classic butterfly-shaped rash across the cheeks and bridge of the nose is the most recognized skin symptom of SLE.

Smeltzer and Bare (2003) reported that lesions tend to worsen during intensification of systemic disease, which can be exacerbated by artificial ultraviolet light or sunlight. Additionally, crops of oral ulcers at the hard palate and mucosa may occur. Musculoskeletal involvement, including arthralgias, arthritis, and synovitis, is marked by pain on movement accompanied by morning stiffness, tenderness, and joint swelling (Smeltzer ; Bare, 2003). Boumpas et al. (1995) noted that valvular heart disease is caused by fibrinoid degeneration of valve cusps, verrucous vegetations, vasculitis, fibrotic scarring, antiphospholipid antibodies, valvulitis, and rupture of chordae tendineae. They also expanded the range of lupus-related valvulopathies to include valve leaflet thickening with or without lesions of Libman-Sacks endocarditis and valve dysfunction.

Valvular abnormalities, which may require valve replacement, can cause significant

hemodynamic lesions (Boumpas et al., 1995), as well as common pericarditis (Smeltzer ; Bare, 2003).

Various risk factors, such as hyperlipidemia, hypertension, and obesity are associated with atherosclerosis. Acute damage to the alveolar-capillary unit leads to pulmonary involvement in the form of acute lupus pneumonitis and alveolar hemorrhage. Chest radiography reveals patchy alveolar infiltrates while symptoms include dyspnea with hypoxemia, sudden onset of fevers, and lower hemoglobin levels due to lung bleeding in the case of alveolar hemorrhage syndrome. Studies indicate that elevated plasma levels of complement split products could activate circulating neutrophils leading to reduced oxygenation capacity and acute reversible hypoxemia in the pulmonary vasculature.

Smeltzer and Bare (2003) suggest that pulmonary hypertension may stem from several factors, including vascular occlusion related to lung disease, vasoconstriction, platelet aggregation or thrombosis, and vasculopathy or vasculitis. Moreover, Boumpas et al. (1995) state that autoimmune thrombocytopenia—a hematologic ailment—arises when antiplatelet autoantibodies bind to surface glycoproteins. As a result of this binding, macrophages located in the bone marrow, liver, spleen, and lymph nodes with receptors for the Fc region of immunoglobulin consume antibody-coated platelets.

The kidney's lupus nephritis growth seems to be encouraged by immune complex localization in the kidney, as stated by Smeltzer & Bare in 2003. Anti-DNA autoantibodies' cross-reactivity with glomerular cell surface antigens supports glomerular immune complex formation, which settles in the glomerulus due to normal components of basement membrane and mesangial matrix, according to Boumpas et al. (1995). The proinflammatory immune complex settling near circulation's subendothelial region can cause cellular proliferation, inflammation, necrosis, and fibrosis. Additionally, some autoantibodies may combine with nuclei and participate in glomerular proliferation and proteinuria (Smeltzer & Bare, 2003). Neuropsychiatric lupus-associated primary histopathological

abnormalities are multifocal cerebral cortical microinfarctions resulting from microvascular injury caused by vasculitis, thrombosis, vasculopathy antibody-mediated neuronal cell injury or dysfunction and leukoagglutination (Boumpas et al.).

Antibodies may enter the CNS through a disrupted blood-brain barrier due to vascular injury or through intrathecal production. This may result in various symptoms such as apathy, memory impairment, behavioral changes, loss of intellect or judgment, orientation, agitation, stupor, delirium, or coma. In severe cases, active ongoing neuropsychiatric lupus may cause dementia due to multiple antiphospholipid antibody-induced infarctions. Diagnosis of SLE involves blood tests, physical examination including inspection of the skin for hyperpigmentation or depigmentation, erythematous rashes and plaques, and sensitivity to sunlight. (Boumpas et al., 1995; Mills, 1994; Smeltzer & Bare, 2003).

The examination should include checking for alopecia on the scalp and ulcerations in the mouth and throat (Mills, 1994). To assess cardiovascular health, it is important to listen for pericardial friction rub, which may be linked to pleural effusions and myocarditis (Smeltzer & Bare, 2003). Pleural infiltrations and effusions, which can cause respiratory insufficiency, can be identified through abnormal lung sounds and seen on CXR (Mills, 1994). Vascular involvement may be indicated by purpuric lesions, erythematous and necrotic papular. Physical examination may reveal edema, tenderness, joint swelling, warmth, stiffness, and pain on movement. Classic symptoms include fatigue, weight loss and fever, as well as pericarditis, arthritis, and pleurisy (Smeltzer & Bare, 2003).

Neurologic assessment is carried out to identify changes in behavior and the Central Nervous System (Mills, 1994). Blood tests can detect the presence of antinuclear antibodies, leukocytosis or leucopenia, anemia and thrombocytopenia while urinalysis may identify creatinine and hematuria (Smeltzer & Bare, 2003). Medical Management involves preventing

therapy-related complications, minimizing the risk of acute illness, avoiding progressive organ function loss, and reducing disease-related disabilities (Boumpas et al, 1995). The management of SLE entails regular monitoring to assess therapeutic effectiveness and disease activity. Medication for SLE is based on the premise that local tissue inflammation is reduced through targeted immune response suppression (Smeltzer & Bare, 2003).

The NSAIDs that are used to treat minor clinical manifestations of SLE are usually combined with corticosteroids, which are the most valuable drug available for treating the disease (Boumpas et al, 1995). Antimalarial drugs are also used to effectively manage mild systemic, musculoskeletal, and cutaneous features of SLE (Smeltzer & Bare, 2003). Immunosuppressive agents, such as purine analogs and alkylating agents, are also utilized because of their effect on immune function (Boumpas et al, 1995; Smeltzer & Bare, 2003). In terms of nursing management, people with SLE often experience body image disturbance, discomfort, impaired skin integrity, fatigue, and a lack of knowledge when it comes to making self-management decisions (Doenges & Moorhouse, 1991).

Patients with a disease or undergoing its management may experience significant distress and appearance alterations. Support groups can offer information, management tips, and social support to assist patients (Smeltzer & Bare, 2003). It's essential to educate patients on protecting themselves with clothing and sunscreen and avoiding exposure (Doenges ; Moorhouse, 1991). In cases of increased risk for cardiovascular diseases, dietary consultation is necessary for dietary recommendations. Nurses can guide patients on the importance of continuing prescribed medications despite side effects and changes (Doenges ; Moorhouse, 1991). To minimize systemic risks, patients should regularly undergo screenings, monitoring and participate in health promotion exercises (Doenges ; Moorhouse, 1991;

Smeltzer ; Bare, 2003).