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Lupus Midterm

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Submitted By AnnieCrane
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The Lupus Foundation of America approximates that there are around 1.5 million Americans affected by a form of lupus (Rooney 54). There are two main factions of lupus: systemic lupus erythematosus (SLE) and discoid lupus erythematosus (DLE). The popular depiction of lupus as a disease associated with lesions and superficial symptoms is not necessarily an accurate portrait. Although Lupus Erythematosus gets its name from the Latin word lupus (wolf) because the lesions resembles the pattern of a wolf bite, the most common form of the disease is SLE which does not require lesions as a criteria for diagnosis (Rooney 56). The underlying concern that both DLE and SLE share is their label as an autoimmune disease. Autoimmune diseases work by attacking self antigens and tissues as if they were foreign (McKinley, O’Loughlin and Bidle 856). By analyzing a deconstructed look at lupus we hope to gain an insight into lupus’ pathological effect on the body and its relation to the immune system.
SLE occurs when the body begins to attack its own tissues without known cause. Although there is not a definitive known cause for SLE, autoantibodies can combine to form immune complexes which can effectively damage internal tissue and the hyperactivity of b-cells contributes to the symptoms (Pullen, Brewer and Ballard 23) (Porth 1422). Genetic predisposition to SLE is evidenced by an increased concordance rate in twins (10-fold), increased incidences within family members (10%-16%), and increased frequency of certain gene alleles in population based studies (Tsao and Wallace 378).There are a variety of factors that can contribute to an exaggerated immune response in an SLE patient including hormonal changes, stress, UV exposure, and medications (Pullen, Brewer and Ballard 24). This exaggerated immune response can cause a cell-mediated reaction that damages the epidermal tissue (see fig. 1) (Rooney 56). Renal involvement is a serious complication caused primarily by disposition of circulating immune complexes in the glomerular basement membrane with cellular infiltrates (McKinley, O'Loughlin and Bidle 856). Because of the wide variety of symptoms associated with SLE it has garnered the name “the great imitator” in regard to its capacity to affect almost any of the body systems including the central nervous system (CNS), the lungs, the kidneys, and the cardiovascular system amongst others (Porth 1423).
DLE commonly occurs in women after their late 30s (McCance, Huether and Brashers 1659).Some patients who originally present with DLE will develop SLE (Rooney 57) .There are three subcategories of DLE: acute, subacute, and chronic. All categories are noted by their lesions, which come in many sizes and can stand alone or may flare up in patches (McCance, Huether and Brashers 1659). The face is a common area for lesion flare ups and a butterfly pattern is common amongst patients experiencing DLE (McCance, Huether and Brashers 1659) (Pullen, Brewer and Ballard 25). The malar rash that squares the nasal labial fold is a suggestive feature but not pathognomonic. Maculopapular rashes are frequent and can occur anywhere but typically appear on sun exposed skin. Nails and hair can be involved with red, cracked cuticles, periungual telangiectasias, and patchy or diffuse alopecia (McCance, Huether and Brashers 1658). Raynaud Phenomenon, vasospasms of the blood vessels, causes cool hands and feet with pain and characteristic tricolor change (McKinley, O'Loughlin and Bidle 855). The cause of DLE is attributed to the development of self-reactive t and b-cells as well as a decrease in regulatory t-cells and increased proinflammatory cytokines. This response is thought to be generated by a response to an unknown antigen or the sensitivity to UV wavelengths (McCance, Huether and Brashers 1659).
The diagnostic criteria of SLE and DLE are profoundly different. Diagnosis of DLE is reached by taking a biopsy of the lesions. Immunoflorescent observation of the biopsy will reveal deposits of immunoglobulins, particularly IgM which can confirm the presence of DLE (McCance, Huether and Brashers 1660). Conversely, SLE has 11 diagnostic criteria established by the American College of Rheumatology (Rooney 56). In order to be diagnosed as having SLE the patient must present with at least 4 of the 11 criteria (Pullen, Brewer and Ballard 24). There are a select group of tests that can be utilized in order to clarify the presence of SLE; these include the serum antinuclear antibody (ANA), Anti-Smith, Anti-double-stranded DNA (anti-dsDNA), and Antiphospholipid (APL) tests (Rooney 57). The ANA test is used to detect antibodies that will mistake the nuclei of self-cells for foreign invaders and attack (Rooney 57). 95% of patients with SLE test positive for high ANA levels (Porth 1424).
Treatments for DLE and SLE vary, there is no cure for either type of lupus but there are medications that can be prescribed in order to prevent and manage symptom flares. NSAIDS can control inflammation, and Corticosteroids are used to treat the renal and CNS symptom of SLE. In high doses Corticosteroids can be used for acute symptoms (Porth 1424). Antimalarial drugs can help reduce many of the symptoms of SLE such as arthritis, rashes, fatigue, and fever but take several months to take effect (Rooney 58). Cytotoxic and immunosuppressive drugs are usually used to suppress the immune system in extreme cases such as an organ transplant, but they can be effective in suppressing the exaggerated immune responses that occur in patients with SLE as well.
This paper demonstrated the various ways lupus presents in patients and the diverse methods used to treat this disease. By using research to take a closer look into the pathology of lupus in its many forms the paper was able to address the two leading types of lupus as well as their symptoms, diagnostic processes, and treatment. Although there is no definitive information on the pathology of lupus in relation to why it occurs, the abundance of knowledge of the complications it causes and how it affects the immune system allows future medical professionals to continuously gain more understanding.

Figure 1. Effect of Lupus During Immune Reaction (Rooney 56)

Works Cited
McCance, Katheryn L., et al. Pathophysiology: The Biologic Basis for Disease in Adults and Children. 6th. Maryland Heights, Missouri: Mosby Elsevier, 2010.
McKinley, Michael P., Valerie D. O'Loughlin and Theresa S. Bidle. Anatomy & Physiology: An Integrative Approach. New York: McGraw-Hill, 2013.
Porth, Carol M. Pathophysiology: Concepts of Altered Health States. 7th. Philadelphia, PA: Lippincott Williams & Wilkins, 2005.
Pullen, Jr., Richard L., Sharon Brewer and Adonna Ballard. "Putting a Face on Systeic Lupus Erythematosus." Nursing2009 39.8 (2009): 23-28.
Rooney, Joan. "Systemic Lupus Erythematosus: Unmasking a Great Imitator." Nursing2005 35.11 (2005): 54-60.
Tsao, B. and D Wallace. "Genetics of Systemic Lupus Erythematosus." Current Opinion in Rheumatology 9.5 (1997): 377-379. Document.

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