Nurs 6501 week 2 discussion – Erythematosus & Psoriasis Essays
Systemic Lupus Erythematosus & Psoriasis
This week’s discussion will deal with the pathophysisology of Systemic Lupus Erythmatosus (SLE) and Psoriasis. The discussion will entail the compensatory mechanisms, maladaptive and physiological responses of the two disorders. The age inference with regards to the pathophysiology of both SLE and Psoriasis will be reviewed.
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Pathophysiology of Systemic Lupus Erythematosus
Systemic Lupus Erythmatosus originates from autoimmune system and is a multisystem inflammatory disease. During the disease state, there is production of huge varieties of auto antibodies against nucleic acids (single and double stranded DNA), erythrocytes, coagulation proteins, lymphocytes, platelets, and many other self- proteins which causes inflammation, pain, and damage in various parts of the body(Lupus Foundation of America, 2012). These autoimmune reactions are directed against constituents of the cell nucleus that is antinuclear antibodies, particularly DNA, and as a result, the circulating immune complexes containing antibody against DNA are deposited in the basement membranes of capillaries in the kidneys, heart, skin, brain, and joints. Once the complement is activated, inflammation occurs. Nurs 6501 week 2 discussion – Erythematosus & Psoriasis Essays It is imperative for advanced practice nurses to know that the specific manifestations of SLE depends on type of cell or organs that is involved (Lewis, Heitkemper, Dirksen, Bucher, & Camera, 2011)
Pathophysiology of Psoriasis
Psoriasis is a chronic dermatitis and relapsing inflammatory disease involving excessively rapid turnover of epidermal cells. During the inflammatory cascade of this disorder, there is secretion of multiple inflammatory mediators( interferon, tumor necrosis factor- alpha), and cytokines (interleukin-12, 13, 17) due to complex interactions between macrophages, fibroblasts, dendritic cells, natural killer cells, T helper cells, and regulatory T cells (Huether &McCance, 2017) Nurs 6501 week 2 discussion – Erythematosus & Psoriasis Essays.
Variation in Physiological Responses
SLE is extremely variable in its severity, ranging from a relatively mild disorder to a rapidly progressive one affecting multiple body system due to accumulation of circulating immune complexes (Lupus Foundation of America, 2012), whereas psoriasis can be mild, moderate, or severe, depending on the size, distribution, and inflammation of the lesions implicating mostly the dermis and epidermis due to cellular hyper-proliferation, altered keratinocyte differentiation, and expanded dermal vasculature (Huether & McCance, 2017). The most commonly affected tissues by the SLE are the skin and muscle, the lining of the lungs, heart, nervous tissue, and the kidneys whereas psoriasis mostly affects the skin, scalp, and the nails. Generalized complaints like fever, weight loss, arthralgia, and excessive fatigue may precede an exacerbation of SLE activity, whereas a well-demarcated, thick, silvery, scaly erythematous plaque surrounded by normal skin is the most common clinical manifestation of psoriasis (Lewis et al., 2011). It is very crucial that advanced practice nurses should familiarize themselves with this variation for proper diagnosis and treatment. Nurs 6501 week 2 discussion – Erythematosus & Psoriasis Essays.
Patient Factor: Age
According to Huether and McCance (2017), psoriasis can occur at any age, but the onset is generally established by forty years of age. Any onset of psoriasis at later stage in life is less familial and much secondary to co-morbidities, like obesity, smoking, high blood pressure, and diabetes. With SLE, symptoms and diagnosis occur most often when women are in their childbearing years, between the ages of 15 and 44. Symptoms of lupus will occur before age 18 in 15 percent of the people who are later diagnosed with the disease (Lupus Foundation of America, 2012) Nurs 6501 week 2 discussion – Erythematosus & Psoriasis Essays.
Conclusion
Both SLE and psoriasis are both inflammatory disorders, but psoriasis mostly affect the skin while SLE is multiple system based. Both disorders involve complex interactions to precipitate a pathological responses of the disease state. Age is cited in different research findings as one of the factors that implicate the pathophysiology of both SLE and psoriasis.
References
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
Lewis, S. L., Heitkemper, M.M., Dirksen, S. R., & Bucher, L., & Camera, I. (2011). Medical-
surgical nursing: Assessment and management of clinical problems (7th ed.). St. Louis,
Missouri: Mosby. Nurs 6501 week 2 discussion – Erythematosus & Psoriasis Essays
Lupus Foundation of America. (2012).What are the risk factors for developing lupus? Retrieved
from http://www.lupus.org/answers/entry/risks-for-developing-lupus
Lupus Foundation of America. (2012).What happens in autoimmune diseases like lupus?
Retrieved from http://www.lupus.org/answers/entry/what-happens-in-autoimmune-diseases-like-lupus
NURS 6501
Week 2, Discussion 2, Initial Post
Osteoarthritis
Osteoarthritis (OA) is joint inflammation related to the destruction of cartilage. There can be genetic factors involved in OA, but the primary mechanism of damage in this condition is an excess of wear (Huether & McCance, 2012). The cartilage that lines the joints is worn away, and the bones begin to rub against one another with joint movement causing friction and bone breakdown, which in turn prompts bone growth in the form of osteophytes or bone spurs. There are also some proteolytic actors in play that aid in the degeneration of the cartilage (Vincent, Conrad, Fregly, & Vincent, 2012). Nurs 6501 week 2 discussion – Erythematosus & Psoriasis Essays.
Primary treatment of OA is pain control and lifestyle modifications including resting inflamed joints, weight loss if indicated, and range of motion exercises to promote joint capsule health. Treatment for severe cases of OA include surgical procedures to address bone spurs, manage/correct joint deformities, and to replace entire joints when necessary.
Rheumatoid Arthritis
Rheumatoid arthritis (RA), while causing similar joint damage to that of OA, is an autoimmune disorder rather than an age-related disorder (Mcphee & Hammer, 2010). Pannus, or granulation tissue forms in response to inflammation of the synovium. Ankylosing, or fixation of the joint in an abnormal position occurs due to destruction of the articular cartilage and subchondral bone. Rheumatoid factor, IgM antibody and neutrophils are the primary autoimmune culprits responsible for the destruction of tissue in RA (Choy, 2012). Treatment consists of control and reduction of inflammation. Disease modifying anti-rheumatic drugs help decrease joint damage. Anti-inflammatory meds and steroids can help with the pain and inflammation. Nurs 6501 week 2 discussion – Erythematosus & Psoriasis Essays.
Patient Factors
Genetics plays a role in both OA and RA. Continued research is necessary to increase understanding of the genetics impact of both OA (Vincent, Conrad, Fregly, & Vincent, 2012) and RA (Choy, 2012). Advancement of genetic research related to OA and RA could lead to new treatments and even the potential of preventative therapies/treatments.
References
Choy, E. (2012). Understanding the dynamics: Pathways involved in the pathogenesis of rheumatoid arthritis. Rheumatology, 51, v3-v11. doi:10.1093/rheumatology/kes113
Huether, S., & McCance, K. (2012). Understanding Pathophysiology (5th ed.). St. Louis, Missouri: Elsevier.
Mcphee, S. J., & Hammer, G. D. (2010). Pathophysiology of disease: An introducion to clinical medicine (6th ed.). Boston: McGraw-Hill.
Vincent, K. R., Conrad, B. P., Fregly, B. J., & Vincent, H. K. (2012). The pathophysiology of osteoarthritis: A mechanical perspective on the knee joint. Physical Medicine and Rehabilitation, 4(5 0), S3-S9. doi:10.1016/j.pmrj.2012.01.020 Nurs 6501 week 2 discussion – Erythematosus & Psoriasis Essays