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Systemic Lupus Erythematous (SLE) is a complex chronic autoimmune inflammatory disease of unknown cause, characterized by a variety of autoantibodies that attack self-components. It is mostly characterized by autoantibodies that attack nuclear antigens (McCance & Huether, 2014). Explain why the pathology is a possibility for this patient.
Why do the clinical manifestations this patient has make you consider the pathophysiological problem? SLE is a chronic inflammatory disease that can attack any organ system, but it often attacks the joints, blood cells, and the nervous system. This patient presents with neurological symptoms of dizziness, paresthesia, and tingling in the lower extremities. Hematological symptoms include signs of anemia with dizziness, fatigue, a pale retinal background, pale conjunctiva, pale nasal mucosa, a pale posterior pharynx, coldness in the lower extremities, and a beefy red tongue. Musculoskeletal joint pain or arthritis is a common feature seen in SLE. The female sex is most common for SLE and a history of arthritis is a precursor. Antibodies can be present for ten or more years before symptoms emerge, which could indicate why she is now presenting with symptoms.
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Clinical manifestations and their pathophysiology. SLE affects all, or some, systems of the body. Pinpointing what kinds of cells are causing damage is very difficult, which is why having four or more clinical findings with the presence of antinuclear antibodies confirms SLE. Dizziness can result from autoantibodies attacking the brain tissue, specifically when damage occurs to the labyrinth, central vestibular structure, or vestibular nerve in the brainstem. Dizziness can also occur from anemia due to the lack of circulating oxygen in the body (Di Stadio & Ralli, 2017).
Paresthesia of the lower extremities can result from autoantibodies attacking nerve tissue, specifically the myelin sheath protecting the nerves. This can cause numbness, tingling, or even burning in the extremities. Fatigue, pallor of mucosal tissues, and a beefy red tongue are classic signs of anemia due to reduced oxygen circulation and a low number of red blood cells. The decrease in oxygen can also cause damage to many cells, resulting in apoptosis (Giannouli, Voulgarelis, Ziakas, & Tzioufas, 2005).
Fatigue is one of the most common clinical manifestations of SLE and comes from a variety of affected systems but is mostly due to the antibodies attacking self-cells. Ninety percent of SLE cases affect the female gender. There is no known reason why, but it is suspected that hormones play a role in onset and flare-ups (McCance & Huether, 2014).
Arthritis is another common clinical finding in SLE and results from the synovitis and inflammation of the joint capsule, ligaments, and tendons. In SLE, coldness in the hands and feet, known as Raynaud’s phenomenon, is usually triggered by cold temperatures or emotional stress, and results from the vasoconstriction of vessels coupled with anemia and a low oxygen count (Fardoun, Nassif, Issa, Baydoun, & Eid, 2016).
What other information would you need to know to help with this diagnosis? An examination of the skin would be helpful to determine if there is a malar or discoid rash. A urinalysis would be useful to detect any renal injury, specifically looking for proteinuria greater than 0.05 g/day, RBCs, and hemoglobin. Blood work would help determine the presence of a hematologic disorder, looking for hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia (McCance & Huether, 2014). The presence of serum values would determine an immunologic disorder; looking for anti-DNA, anti-Sm, or antiphospholipid antibodies (McCance & Huether, 2014). Lastly, the presence of an antinuclear antibody (ANA) would confirm SLE.
What causes it? The specific cause of SLE is unknown. It is believed that many things contribute to the onset of the disease, including genetics, epigenetics, ethnicity, immunoregulatory, environmental, and hormonal factors (McCance & Huether, 2014). SLE patients experience many immune disruptions.
Antibodies can be present for years before any symptoms occur. The mechanisms of SLE are still mostly hypothesized. One theory is that a defect in apoptosis causes increased cellular death causing the immune system to activate and attack itself. As antigens redistribute, nuclear antigens and plasma appear as nucleosomes. Lymphocytes then target these antigens. The apoptotic cell remnants are not cleared effectively and antigen and immune complex continuation occurs (Giannouli et al., 2005).
Patients with SLE have T cells that have defects in effector function and signaling. The clinical manifestations of SLE are caused by immune complexes combined with antigens in different tissues or the effects of antibodies on cell surface factors, thereby causing inflammation. The antigen-antibody unit resides on glomerular basement membranes. Any form of trauma will increase the circulation of DNA; the liver typically removes damaged DNA but the immune complexes slow the process, resulting in an accumulation in the kidneys.
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