Respond on to  two different days who selected different immune

Respond on to  two different days who selected different immune disorders and/or factors than you, in the following ways: Share insights on how the factor you selected impacts the pathophysiology of the immune disorder your colleague selected. Expand on your colleague’s posting by providing additional insights or contrasting perspectives based on readings and evidence.                                                        Main Post   Maladaptive Responses to Immune Disorders       For this week’s discussion post, we will discuss the maladaptive and physiological responses of HIV and Lupus.  We will first discuss the pathophysiology of each and then further break the disorders down.  We will review how the gender factor might impact the pathophysiology of the disease. Pathophysiology of HIV      Human Immunodeficiency Virus (HIV) is the viral infection that leads to Acquired Immune Deficiency Syndrome (AIDS).    HIV is a blood-borne pathogen.  Modes of transmission for HIV are IV drug abuse, blood product transfusion or transmission, maternal-child transmission, and both homosexual and heterosexual populations can be affected.  HIV seeks and destroys the CD-4+ Th cells.  CD-4+ cells are essential or the cytotoxic T cell and plasma cell development.  Because of the CD-4+ destruction, there is a suppressed immune response which leads to AIDS (Huether & McCance, 2017).  Maladaptive Response and the Female Factor      Maladaptive responses to HIV are anxiety, disturbed thought processes, imbalanced nutrition, infective coping, social isolation, this is just a few.  Women make up more than half the cases worldwide.  Approximately 50,000 new cases of HIV present each year in the United States, 25% of these new cases are from heterosexual relationships with two-thirds of that percentage being women, highest among black women (Huether & McCance, 2017). Pathophysiology of Lupus      Autoantibodies target specific self-antigens known as the initiation phase.  Environmental factors, such as sunlight, may be the cause for these triggers or viral infections like Epstein-Barr. SLE has long been thought to have an active genetic link.  In an average individual, apoptotic cells self destruct but for individuals with systemic lupus erythema (SLE) effectively immunize themselves with bad cells from their tissue.  The body fights itself instead of excreting the bad cells.  Propagation is the second phase of SLE; this phase involves the inflammatory response and tissue damage and can affect the heart, kidneys, brain, skin, and joints.  Thirdly is the flare stage and includes a quicker and more vigorous immune response; this stage may provoke disease flares (Hammer & McPhee, 2019). Maladaptive Response and the Female Factor      Maladaptive responses to SLE might be altered image issues, fatigue related to chronic inflammation, and impaired skin integrity related to skin rash.  Women are ten times more likely to develop SLE than men.  African Americans have the highest risk, followed by Hispanics, Asian Americans, and Native Americans.  The primary age to develop SLE is between 20-40 years old (the childbearing years) with the most prevalent age being around 30 (Lewis, Bucher, Heitkemper, & Harding, 2017). References Hammer, G. D., & McPhee, S. J. (2019). Pathophysiology of disease: An introduction to clinical medicine (8th  ed.). New York, NY: McGraw-Hill Education. Huether, S. E., & McCance, K. L. (2017). Understanding  pathophysiology (6th ed.). St. Louis, MO: Mosby. Lewis, S.L., Bucher, L., Heitkemper, M.M., & Harding, M.M.  (2017) Medical-surgical nuring assessment and management of clinical problems (10th ed.).  St. Louis, MO:  Elsevier

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